Adolescent pregnancy is a major public health challenge for many industrialised countries and is associated with significant medical, nutritional, social and economic risk for mothers and their infants. Despite this, relatively little is known about the nutrient intakes of adolescents during pregnancy. The aim of this study is to review the current evidence relating to the dietary assessment of pregnant adolescents living in industrialised countries. Nine papers were identified that fulfilled the inclusion criteria, seven of which were conducted in the USA. Mean nutrient intakes were compared with the most recent US dietary reference intakes (DRI) for pregnant adolescents. Despite the poor quality of the majority of studies, there appeared to be some consensus to suggest that the nutrient intakes of pregnant adolescents were below the DRI for energy, iron, folate, calcium, vitamin E and magnesium, nutrients which are recognised to be vital for fetal growth and development during pregnancy. Modest differences were observed in nutrient intake between trimesters and age groups. Current research is limited by sampling and measurement bias, and research is urgently required to address these limitations. Further consideration should also be made of the influence of age and of role of socio-economic support on pregnant adolescents' nutrient intake. The achievement of improved nutrition in pregnancy among adolescents requires multidisciplinary collaborations of adolescent health care providers, academics, professional organisations, policy makers, industry and service users. Only once this is achieved can adolescent nutrition, and adolescent nutrition in pregnancy, be significantly and sustainably optimised.

Pancreatic polypeptide (PP) is a gut hormone released from the pancreas in response to food ingestion and remains elevated for up to 6 h postprandially. Plasma levels are elevated in patients with pancreatic tumours. An intravenous infusion of PP has been reported to reduce food intake in man, suggesting that PP is a satiety hormone. We investigated whether a lower infusion rate of PP would induce significant alterations in energy intake. The study was randomised and double-blinded. Fourteen lean fasted volunteers (five men and nine women) received 90 min infusions of PP (5 pmol/kg per min) and saline on two separate days. The dose chosen was half that used in a previous human study which reported a decrease in appetite but at supra-physiological levels of PP. One hour after the end of the infusion, a buffet lunch was served and energy intake measured. PP infusion was associated with a significant 11 % reduction in energy intake compared with saline (2440 (se 200) v. 2730 (se 180) kJ; P < 0·05). Preprandial hunger as assessed by a visual analogue score was decreased in the PP-treated group compared to saline. These effects were achieved with plasma levels of PP within the pathophysiological range of pancreatic tumours.

High alcohol consumption is related to colorectal cancer (CRC). Our objective was to study associations between alcohol consumption and risk of CRC according to characteristics of aetiological pathways: the chromosomal instability (CIN) and the microsatellite instability (MIN) pathway. We classified CIN+ tumours (tumours with either a truncating APC mutation, an activating K-ras mutation or overexpression of p53), MIN+ tumours (tumours lacking hMLH1 expression) and CIN− /MIN−  tumours (tumours without these defects). In the Netherlands Cohort Study on diet and cancer, 120 852 men and women, aged 55–69 years, completed a questionnaire on risk factors for cancer at baseline (1986). Case–cohort analyses were conducted using 573 CRC cases with complete data after 7·3 years of follow-up, excluding the first 2·3 years. Adjusted incidence rate ratios (RR) and 95 % confidence intervals (CI) were estimated. Compared with abstaining, alcohol consumption of ≥ 30 g/d was positively associated with the risk of CRC irrespective of genetic or molecular aberrations present, although statistical significance was not reached (RR 1·35 (95 % CI 0·9–2·0) for the CIN+ tumours, RR 1·59 (95 % CI 0·4–5·8) for the MIN+ tumours and RR 1.15 (95 % CI 0·5–2·7) for the CIN− /MIN−  tumours). Beer, wine and liquor consumption were, independent of their alcoholic content, not consistently associated with the risk of CRC within the defined subgroups. In conclusion, our results indicate that a daily alcohol consumption of ≥ 30 g is associated with an increase in risk of CRC, independent of the presence or absence of the studied characteristics of different aetiological pathways.

Epidemiological studies and experimental models show that maternal nutritional constraint during pregnancy alters the metabolic phenotype of the offspring and that this can be passed to subsequent generations. In the rat, induction of an altered metabolic phenotype in the liver of the F1 generation by feeding a protein-restricted diet (PRD) during pregnancy involves the altered methylation of specific gene promoters. We therefore investigated whether the altered methylation of PPARα and glucocorticoid receptor (GR) promoters was passed to the F2 generation. Females rats (F0) were fed a reference diet (180 g/kg protein) or PRD (90 g/kg protein) throughout gestation, and AIN-76A during lactation. The F1 offspring were weaned onto AIN-76A. F1 females were mated and fed AIN-76A throughout pregnancy and lactation. F1 and F2 males were killed on postnatal day 80. Hepatic PPARα and GR promoter methylation was significantly (P < 0·05) lower in the PRD group in the F1 (PPARα 8 %, GR 10 %) and F2 (PPARα 11 %, GR 8 %) generations. There were trends (P < 0·1) towards a higher expression of PPARα, GR, acyl-CoA oxidase and phosphoenolpyruvate carboxykinase (PEPCK) in the F1 and F2 males, although this was significant only for PEPCK. These data show for the first time that the altered methylation of gene promoters induced in the F1 generation by maternal protein restriction during pregnancy is transmitted to the F2 generation. This may represent a mechanism for the transmission of induced phenotypes between generations.

Lutein is assumed to protect the human retina from blue light and oxidative stress and diminish the incidence of age-related macular degeneration. This antioxidant is commonly ingested with other dietary antioxidants. The aim of the present study was to assess whether the main dietary antioxidants, i.e. carotenoids, polyphenols and vitamins C and E, affect lutein absorption. We measured the effect of adding a mixture of antioxidants (500 mg vitamin C, 67 mg (100 IU) vitamin E and 1 g polyphenols) to a lutein-containing meal (18 mg) on the postprandial lutein response in the chylomicron-rich fraction in eight healthy men. Lutein response was weakest ( − 23 %; P = 0·07) after ingestion of the meal containing antioxidants (21·9 (sem 4·6) v. 28·4 (sem 7·2) nmol × h/l). To assess the effect of each class of antioxidants and potential interactions, we subsequently evaluated the effect of various combinations of antioxidants on lutein uptake by human intestinal Caco-2 TC-7 cells. A full factorial design showed that both a mixture of polyphenols (gallic acid, caffeic acid, (+)-catechin and naringenin) and a mixture of carotenoids (lycopene plus β-carotene) significantly (P < 0·05) impaired lutein uptake by ( − 10 to − 30 %), while vitamins C and E had no significant effect. Subsequent experiments showed that the aglycone flavanone naringenin was the only polyphenol responsible for the effect of the polyphenol mixture, and that the carotenoid effect was not carotenoid species-dependent. Taken together, the present results suggest that lutein absorption is not markedly affected by physiological concentrations of vitamins C and E but can be impaired by carotenoids and naringenin.

Oxidative modification of LDL is causally involved in the development of atherosclerosis and occurs in vivo in the blood as well as within the vascular wall. The present study attempted to explore whether polyphenolic flavonoids influence monocyte-endothelium interaction and lectin-like oxidised LDL receptor 1 (LOX-1) expression involved in the early development of atherosclerosis. The flavones luteolin and apigenin inhibited THP-1 cell adhesion onto oxidised LDL-activated human umbilical vein endothelial cells (HUVEC), while the flavanols of ( − )epigallocatechin gallate and (+)catechin, the flavonols of quercetin and rutin, and the flavanones of naringin, naringenin, hesperidin and hesperetin did not have such effects. Consistently, Western blot analysis revealed that the flavones at 25 μm dramatically and significantly abolished HUVEC expression of vascular cell adhesion molecule-1 and E-selectin evidently enhanced by oxidised LDL; these inhibitory effects were exerted by drastically down regulating mRNA levels of these cell adhesion molecules. In addition, quercetin and luteolin significantly attenuated expression of LOX-1 protein up regulated in oxidised LDL-activated HUVEC with a fall in transcriptional mRNA levels of LOX-1. In addition, quercetin and luteolin clearly blunted oxidised LDL uptake by HUVEC treated with oxidised LDL. The results demonstrate that the flavones luteolin and apigenin as well as quercetin were effective in the different initial steps of atherosclerosis process by inhibiting oxidised LDL-induced endothelial monocyte adhesion and/or oxidised LDL uptake. Therefore, certain flavonoids qualify as anti-atherogenic agents in LDL systems, which may have implications for strategies attenuating endothelial dysfunction-related atherosclerosis.

p-Coumaric acid (3-(4-hydroxyphenyl)-2-propenoic acid; 4CA), is a ubiquitous plant metabolite with antioxidant and anti-inflammatory properties. The antiplatelet activity of this compound was analysed both ex vivo and in vitro. 4-CA, administered to rabbits for 2 weeks at the dose of 5 mg/kg, mixed with food, inhibited ADP-induced platelet aggregation without affecting blood coagulation. This effect was associated with a marked increase in plasma antioxidant activity, measured as ferric reducing ability of plasma, and with the reduction of thromboxane B2 production. The antiplatelet effect was confirmed by in vitro experiments on human blood: 4CA (500 μm and 1 mm) reduced ADP-induced platelet aggregation (55·2 (se 4·01) % and 35·6 (se 2·35) % relative to basal level, respectively). 4CA was able to modify platelet function, measured with PFA-100™, a shear-inducing device that simulates primary haemostasis. 4CA interfered also with arachidonic acid cascade, reducing thromboxane B2 production and lipopolysaccharide-induced prostaglandin E2 generation (ic50 371 and 126 μm, respectively). The data show that 4CA is an antioxidant compound with good antiplatelet activity at doses that can be obtained with dietary intervention, suggesting possible applications for primary prevention of vascular disease.

The main objective of the present study was to examine the effects of dehydroepiandrosterone (DHEA) on the digestive efficiency of dietary protein and fat. Second, we analysed the specific changes in muscle composition induced by the hormone. DHEA was given in the diet (0·5 %, w/w) to 75-week-old, high-fat-fed Sprague–Dawley rats (n 11) for 13 weeks; age- and weight-matched rats fed on the same diet without DHEA supplementation were used as controls (n 10). To determine dietary protein and fat apparent digestibility coefficients, 1-week 24 h faecal depositions were collected. In parallel, urine N was assessed. These assays were performed twice, in the short term (2-week treatment) and in the long term (13-week treatment). Body and gastrocnemius muscle compositions were also analysed. The present results show that DHEA decreased energy intake, body weight, body fat, adipocyte size and number (P < 0·001). The feed efficiency ratio indicates that DHEA-treated rats were less efficient in transforming nutrients fed into their own biomass. Also, a short-term reduction in protein digestibility (P < 0·05) and in body-protein degradation (P < 0·01) was found in DHEA-treated rats, resulting in an increased content of body protein (P < 0·05). Gastrocnemius muscles were smaller, as a result of fat (P < 0·05) but not protein reduction. In conclusion, we confirm the slimming effect of DHEA and, for the first time, we demonstrate that DHEA has an effect at the digestive level. The anti-obesity properties of DHEA could be related to a reduction in protein digestibility in the short term and a protective effect on body protein with a selective mass loss from body fat.

Postprandial lipaemia (PL) is associated with the metabolic syndrome, CVD and endothelial dysfunction. Aerobic exercise has been shown to reduce PL. Although resistance exercise is recommended for the improvement of the quality of life, management of body weight and prevention of several disorders, its effect on PL has received little attention. The present study examined the effects of low-volume resistance exercise (LVRE) and high-volume resistance exercise (HVRE) on PL. Ten healthy young men performed three trials, each conducted over 2 d. On the afternoon of day 1, they either refrained from exercise (control), performed LVRE (two sets of eight exercises, twelve repetitions at twelve repetitions maximum (RM) in each set; energy expenditure 0·76 MJ), or performed HVRE (four sets of eight exercises, twelve repetitions at 12RM in each set; energy expenditure 1·40 MJ). On the morning of day 2 they consumed a meal containing 67 kJ/kg body weight, of which 65 % energy was from fat. Blood samples were obtained in the fasted state and for 6 h postprandially. The total area under the TAG curve (AUC; mmol/l × h) was lower (P < 0·05) in HVRE (8·76 (sd 3·20)) and LVRE (9·29 (sd 3·64)) compared with control (11·60 (sd 4·35)). The incremental AUC was lower in HVRE compared with control (3·07 (sd 2·53) v. 5·58 (sd 3·72)), but not different between LVRE (3·86 (sd 2·29)) and control. In conclusion, resistance exercise of 1·40 MJ (four sets – eight exercises – twelve RM) or 0·76 MJ (two sets – eight exercises – twelve RM) before a high-fat meal reduces the total postprandial lipaemic response.

The accretion of methionine and protein as a function of methionine intake was assessed in growing ducks between 22 and 42 d post-hatching. Four graded doses of dl-methionine at 0, 0·5, 1·0 or 1·5 g/kg diet were added to a methionine-limiting basal diet and fed to four replicate groups of four ducks each. The growth and efficiency of food use for growth increased linearly (P < 0·05) as a function of methionine intake. The accretion of body protein increased (P < 0·001) from 87·5 to 182·2 g, and that of methionine from 1616 to 3125 mg, over the 21 d period as dietary methionine increased. The accretion rate of methionine in the body (y, mg/d) as a function of methionine intake (x, mg/d) of ducks fed diets containing supplemental methionine at 0, 0·5, 1·0 or 1·5 g/kg diet from day 22 to day 42 post-hatching gave the regression equation: y = − 148·86 (se 32·558)+0·312 (se 0·0384)X, r2 = 0·8253. For protein accretion rate in the body (y, mg/d) as a function of methionine intake (x, mg/d), the regression equation was: y = − 9782 (se 2204)+19·505 (se 2·5994)x, r2 = 0·8009. There was a linear relationship between methionine (y, mg/d) and protein (x, mg/d) accretion in ducks that was described by the equation y = 12·757 (se 7·4019)+0·01 525 (se 0·00 107)x, r2 = 0·9355. The results of these studies suggest a constant utilisation of methionine over the range 2·4–3·9 g digestible methionine/kg diet, with an efficiency of 31 %. Furthermore, the results suggest a quantitative relationship of 15 mg methionine for every gram of protein accretion.

The metabolism of flavone C-glucosides and p-coumaric acid from antioxidant of bamboo leaves (AOB) in rats is discussed systematically in the present study. Following single oral administration of AOB, p-coumaric acid was detected in plasma but not in gastrointestinal tract extracts and faeces, and the corresponding absorption pharmacokinetic curve at different time points showed a prolonged elimination phase with p-coumaric acid being detected in the kidneys and excreted as its original form (1·80 (sd 0·24) % and 1·90 (sd 0·26) % at 12 and 24 h, respectively). However, the four flavone C-glucosides orientin, homoorientin, vitexin and isovitexin were poorly absorbed in the gastrointestinal tract. More than 50 % recovery of flavone C-glucosides was determined at 12 h and faeces containing these four analytes (21·23 (sd 1·92) %) were excreted at 24 h. These data suggested that the effective time these compounds were in the colon was long enough so that they could exert their antioxidant activity and scavenge free radicals. Besides the excretion of the original forms, moieties of the flavone C-glucosides were hydrolysed by deglycosylation and the opening of the heterocyclic C ring. Some small molecules such as phloroglucinol (PG), hydrocaffeic acid (HCA) and phloretic acid (PA) were detected and identified as metabolites of the flavone C-glucosides. In the present work, we compared the metabolic fate of flavone C-glucosides to that of flavone O-glucosides in rats, and evaluated the absorption, tissue distribution and excretion of flavone C-glucosides in AOB on their metabolism for the first time.

The present study was conducted to determine the effects of α-lipoic acid (ALA) on fatty acid mobilisation and ketone body production in female broiler chickens. In the first experiment, chickens received an intravenous infusion of ALA (0, 25 or 50 mg/kg per h) for 90 min. Blood was drawn at 30 min intervals, and plasma glucose, NEFA, free glycerol and hydroxybutyrate were analysed. In the second experiment, ALA (100 mg/kg per h) was continuously infused to chickens fed or fasted for at least 24 h. Changes in plasma metabolites for 90 min were determined. In the first experiment, as shown by the response area, ALA infusion did not affect plasma glucose but increased (P < 0·05) plasma NEFA, regardless of the dose level. In contrast, plasma hydroxybutyrate was reduced at the lower infusion rate (P < 0·05). No significant changes in plasma free glycerol were observed. In experiment 2, ALA stimulated both plasma glucose (P < 0·01) and NEFA (P < 0·001) and the responses were greater than those of controls, regardless of the feeding state. The interaction between ALA and the feeding condition had a significant effect on plasma hydroxybutyrate (P < 0·01). ALA reduced plasma hydroxybutyrate, and this response was greater in the fasted birds than in those fed. Therefore, the present study found a lowering effect of ALA on plasma hydroxybutyrate level and suggests that the ALA-induced plasma NEFA increment was attributable to decreased hepatic fatty acid oxidation in chickens.

The effects of the type of grass silage and dietary inclusion of fish oil (FO) on the fatty acid profile of bovine intramuscular and subcutaneous adipose tissue were investigated. Eighty Friesian steers were assigned (n 10) to unwilted or wilted silage, and to one of four rations which contained, per kg, 80 g of sunflower oil and either 0, 10, 20 or 40 g of FO replacing lard. Animals were slaughtered after 108 d and the fatty acid profile of the neutral, polar and total lipid fractions of the M. longissimus dorsi, and the total lipid fraction of the subcutaneous adipose tissue were determined. Wilting of grass prior to ensiling increased the concentration of conjugated linoleic acid (CLA) in intramuscular total lipid (P < 0·01), but did not affect the n-6:n-3 PUFA ratio. Increasing FO supply linearly increased (P < 0·05) the concentration of the cis-9, trans-11 and trans-10, cis-12 isomers of CLA and trans-11 18 : 1 predominantly in the neutral lipid fraction of intramuscular total lipid, and linearly decreased the n-6:n-3 PUFA ratio. Wilting of grass prior to ensiling increased the concentration of CLA in subcutaneous adipose tissue (P < 0·001), while increasing FO supply linearly increased the concentration of cis-9, trans-11 CLA. From a human nutrition perspective, increasing the level of FO in the ration or wilting of grass prior to ensiling appear to modify the fatty acid composition of beef muscle favourably. However, the health implications of associated increases in trans fatty acids remain to be elucidated.

Trigonella foenum-graecum (fenugreek) seeds have been documented as a traditional plant treatment for diabetes. In the present study, the antidiabetic properties of a soluble dietary fibre (SDF) fraction of T. foenum-graecum were evaluated. Administration of SDF fraction (0·5 g/kg body weight) to normal, type 1 or type 2 diabetic rats significantly improved oral glucose tolerance. Total remaining unabsorbed sucrose in the gastrointestinal tract of non-diabetic and type 2 diabetic rats, following oral sucrose loading (2·5 g/kg body weight) was significantly increased by T. foenum-graecum (0·5 g/kg body weight). The SDF fraction suppressed the elevation of blood glucose after oral sucrose ingestion in both non-diabetic and type 2 diabetic rats. Intestinal disaccharidase activity and glucose absorption were decreased and gastrointestinal motility increased by the SDF fraction. Daily oral administration of SDF to type 2 diabetic rats for 28 d decreased serum glucose, increased liver glycogen content and enhanced total antioxidant status. Serum insulin and insulin secretion were not affected by the SDF fraction. Glucose transport in 3T3-L1 adipocytes and insulin action were increased by T. foenum-graecum. The present findings indicate that the SDF fraction of T. foenum-graecum seeds exerts antidiabetic effects mediated through inhibition of carbohydrate digestion and absorption, and enhancement of peripheral insulin action.

We studied the effect of several lactic acid bacteria (LAB) on the humoral response of brown trout (Salmo trutta). LAB groups (Lactococcus (Lc.) lactis ssp. lactis, Lactobacillus (Lb.) sakei and Leuconostoc (Leu.) mesenteroides) were administered orally at 106 colony-forming units/g feed to brown trout for 2 weeks, after which fish were switched to an unsupplemented feed. Blood and intestinal samples were taken from the onset of feeding supplemented diets at 1, 2, 3 and 4 weeks. During the LAB-feeding period, Lc. lactis ssp. lactis, Lb. sakei and Leu. mesenteroides persisted in the fish intestines, but the number of LAB slowly decreased in the intestines after changing to the unsupplemented diet. Only Lb. lactis ssp. lactis and Leu. mesenteroides were detected at levels above 1 × 102 colony-forming units/g at the end of the fourth week. In comparison to untreated control fish, the alternative complement activity in the serum was found to be significantly greater in all LAB groups at the end of the second week. Groups supplemented with Lc. lactis ssp. lactis and Leu. mesenteroides exhibited an elevated level of lysozyme activity at the end of the third week, but the group supplemented with Lb. sakei did not exhibit any significant change in lysozyme activity. Serum immunoglobulin levels were higher compared with the control group, but there was no significant difference between the LAB and control groups.

The main objective of the present study was to determine the influence of acute deficits of protein and energy on the blood serum level of interferon-γ, a signature type 1 polarising inflammatory cytokine. In two 14 d experiments, male and female C57BL/6J mice, initial age 19 d, consumed a complete purified diet ad libitum or in restricted daily quantities, or had free access to an isoenergetic purified low-protein diet. A zero-time control group (age 19 d) was included in the second experiment. Serum interferon-γ was assessed in both experiments by sandwich ELISA and, in the second experiment, also by a bioassay based on inhibition of proliferation by WEHI-279 B lymphoma cells. The immunoassay detected interferon-γ inconsistently in all groups (range 0–14 pg/ml; detection limits 1·5 and 0·7 pg/ml in experiments 1 and 2, respectively). By contrast, interferon-γ bioactivity was found in all animals of each group (means 339, 499, 124 and 200 pg/ml in zero-time controls, age-matched controls, low-protein and restricted intake groups, respectively; detection limit, 12 pg/ml), and the mean serum bioactivity of each malnourished group was low compared with the age-matched control (P ≤ 0·05). The present study defines the physiological serum interferon-γ bioactivity of the adolescent mouse. Moreover, to the extent achievable by way of the blood, the results reflect the influence of metabolically diverse forms of acute malnutrition on the polarising type 1 cytokine profile within lymphoid microenvironments wherein immune responses arise. Therefore, the results suggest a mechanism underlying the cell-mediated inflammatory incompetence that characterises acute, prepubescent malnutrition.

Feeding higher levels of dietary animal protein (as casein or red meat) increases colonic DNA damage and thins the colonic mucus barrier in rats. Feeding resistant starch (RS) reverses these changes and increases large bowel SCFA. The present study examined whether high dietary dairy (casein or whey) or plant (soya) proteins had similar adverse effects and whether dietary RS was protective. Adult male rats were fed diets containing 15 or 25 % casein, whey or soya protein with or without 48 % high amylose starch (as a source of RS) for 4 weeks. DNA damage was measured in isolated colonocytes using the comet assay. Higher dietary casein and soya (but not whey) increased colonocyte DNA damage. DNA damage was highest with soya when fed at 15 or 25 % protein without RS. Dietary RS attenuated protein-induced colonocyte DNA damage in all groups but it remained significantly higher in rats fed 25 % soya compared with those fed 15 % protein. Dietary protein level did not affect colonic mucus thickness overall but the barrier was thinner in rats fed high dietary casein. This effect was reversed by feeding RS. Caecal total SCFA and butyrate pools were higher in rats fed RS compared with digestible starch. Caecal and faecal SCFA were unrelated to genetic damage but correlated with mucus thickness. The present data confirm that higher dietary protein affected colonocyte DNA and colonic mucus thickness adversely but that proteins differ in their effects on these indices of colon health. The data show also that these changes were reversed by RS.

Hepcidin plays a major role in iron homeostasis, but understanding its role has been hampered by the absence of analytical methods for quantification in blood. A commercial ELISA has been developed for serum prohepcidin, a hepcidin precursor, and there is interest in its potential use in the clinical and research arena. We investigated the association between serum prohepcidin concentration and iron absorption in healthy men, and its relationship with iron status in men carrying HFE mutations, hereditary haemochromatosis patients, and pregnant women. Iron absorption was determined in thirty healthy men (fifteen wild-type, fifteen C282Y heterozygote) using the stable isotope red cell incorporation technique. Iron status was measured in 138 healthy men (ninety-one wild-type, forty-seven C282Y heterozygote), six hereditary haemochromatosis patients, and thirteen pregnant women. Mean serum prohepcidin concentrations were 214 (sd 118) ng/ml [208 (sd 122) ng/ml in wild-type and 225 (sd 109) ng/ml in C282Y heterozygotes] in healthy men, 177 (sd 36) ng/ml in haemochromatosis patients, and 159 (sd 59) ng/ml in pregnant women. There was no relationship between serum prohepcidin concentration and serum ferritin in any subject groups, nor was it associated with efficiency of iron absorption. Serum prohepcidin is not a useful biomarker for clinical or research purposes.

Long-term supplementation with conjugated linoleic acid (CLA) reduces body fat mass (BFM) and increases or maintains lean body mass (LBM). However, the regional effect of CLA was not studied. The study aimed to evaluate the effect of CLA per region and safety in healthy, overweight and obese adults. A total of 118 subjects (BMI: 28–32 kg/m2) were included in a double blind, placebo-controlled trial. Subjects were randomised into two groups supplemented with either 3·4 g/d CLA or placebo for 6 months. CLA significantly decreased BFM at month 3 (Δ = − 0·9 %, P = 0·016) and at month 6 (Δ = − 3·4 %, P = 0·043) compared with placebo. The reduction in fat mass was located mostly in the legs (Δ = − 0·8 kg, P < 0·001), and in women (Δ = − 1·3 kg, P = 0·046) with BMI >30 kg/m2 (Δ = − 1·9 kg, P = 0·011), compared with placebo. The waist–hip ratio decreased significantly (P = 0·043) compared with placebo. LBM increased (Δ = +0·5 kg, P = 0·049) within the CLA group. Bone mineral content was not affected (P = 0·70). All changes were independent of diet and physical exercise. Safety parameters including blood lipids, inflammatory and diabetogenic markers remained within the normal range. Adverse events did not differ between the groups. It is concluded that supplementation with CLA in healthy, overweight and obese adults decreases BFM in specific regions and is well tolerated.

Due to the growing knowledge about the role of specific fatty acids in health and disease, dietary intake measurements of individual fatty acids or classes of fatty acids are becoming increasingly important. The objective of this study was to evaluate the ability of the Nambour FFQ to estimate intakes of specific fatty acids, particularly PUFA. The study population was a sub-sample of adult participants in a randomised controlled trial of β-carotene and sunscreen in the prevention of skin cancer (n 43). Dietary intake was assessed by a self-administered FFQ and a weighed food record (WFR). Non-fasting blood samples were collected and analysed for plasma phospholipid fatty acids. Median intakes on the FFQ were generally higher than the WFR except for the n-3 PUFA groups, where the FFQ estimated higher intakes. Correlations between the FFQ and WFR were moderate (r 0·32–0·59) except for trans fatty acids (r 0·03). Correlations between each of the dietary assessment methods and the plasma phospholipids were poor for all fatty acids other than the PUFA. Using the methods of triads approach, the FFQ validity coefficients for total n-3 fatty acids, total long chain n-3 fatty acids, EPA, arachidonic acid, docosapentaenoic acid and DHA were 0·50, 0·63, 0·45 and 0·62 and 0·62, respectively. For most fatty acids, the FFQ adequately estimates group mean fatty acid intakes and can adequately rank individuals; however, the ability of this FFQ to estimate trans fatty acids was poor.