The role of flavonoids in CVD is still unclear. In this cross-sectional study we assessed the relation between the intakes of twenty-six flavonoids from five subclasses: flavonols, flavones, flavanones, flavan-3-ols and anthocyanidins, and the mean common carotid artery intima-media thickness (CCA-IMT). The study population consisted of 1380 middle-aged eastern Finnish men for whom the mean CCA-IMT examinations were carried out as a part of the prospective population-based Kuopio Ischaemic Heart Disease Risk Factor Study (KIHD). The mean intake of flavonoids was 128·5 (sd 206·7) mg/d and the mean CCA-IMT was 0·78 (sd 0·17) mm. In the lowest quartile of total flavonoid intake the non-adjusted mean CCA-IMT was 0·79 (sd 0·19) mm, while the mean CCA-IMT was 0·76 (sd 0·15) in the highest quartile (P < 0·001). After adjustment for age, variables related to CCA-IMT measurement, history of atherosclerosis, smoking, BMI, diabetes, systolic blood pressure, serum HDL- and LDL-cholesterol, VO2 max, and intakes of alcohol, SFA, folate, vitamins C and E, the total flavonoid intake was inversely associated with the mean CCA-IMT (P = 0·018). Out of different flavonoid subclasses, flavan-3-ols were inversely associated with CCA-IMT (P = 0·025) after statistical adjustment. There was a trend for an inverse association between intake of flavonols and mean CCA-IMT (P = 0·055). We conclude that high intake of flavonoids is associated with decreased carotid atherosclerosis in middle-aged Finnish men.

In this study, the intake of n-6 and n-3 PUFA of pre-school children in Flanders, Belgium, was evaluated, and recommendations to address the very low intake of long-chain PUFA are presented. Food consumption data (based on parentally reported 3 d dietary records obtained from October 2002 to February 2003) of 661 children (338 boys, 323 girls) between 2·5 and 6·5 years of age and the PUFA concentrations obtained from various food composition databases were used. The actual PUFA intake levels were compared to Belgian, European and American recommendations. Only the intake of linoleic acid (LA) fell within the recommended ranges. Margarine, bread, biscuits and chocolate products contributed most to LA intake. The intake of α-linolenic acid (LNA) was low compared to the recommendations and was obtained mostly from the consumption of margarines and fatty sauces. This resulted in a high LA/LNA ratio. The intake of all long-chain PUFA was far below the recommended levels. Meat and meat products were the most important sources of arachidonic acid. Consumption of fish and other seafood was very low, though these were the most important sources of long-chain n-3 PUFA. In conclusion, Flemish pre-school children should consume more n-3-rich products in order to increase their LNA intake and decrease their LA/LNA ratio. Furthermore, the replacement of meat products rich in SFA by poultry would increase the arachidonic acid intake. As well, fatty fish consumption needs to be increased, as it is a rich source of long-chain n-3 PUFA.

The objectives of the present study were to evaluate the effect of normobaric and hyperbaric O2 (HBO) on plasma antioxidants and biomarkers of oxidative stress in plasma and urine and to investigate the effect of a 4-week vitamin C plus E supplementation on HBO-induced oxidative stress. Nineteen healthy men were exposed to HBO (100 % O2; 240 kPa) before and after 4 weeks' supplementation with 500 mg vitamin C plus 165 mg α-tocopherol equivalents. Exposure to 21 % O2 at 100 kPa served as intra-individual controls (control). Samples for the analysis of plasma antioxidants and oxidative stress biomarkers were collected before and immediately after each treatment. The present results showed that when compared with ‘control’, a single exposure to HBO resulted in a decrease of plasma vitamin C (P = 0·027) and an increase of lipid peroxides (P = 0·0008) and urinary 8-oxo-deoxyguanosine (8-oxodG) excretion (P = 0·006). Oxidative stress was not prevented by a 4-week supplementation with vitamins C and E. HBO-induced changes in plasma parameters correlated with basal antioxidant levels. The increase of urinary 8-oxodG after HBO plus supplementation correlated negatively with vitamin E intake (P = 0·023). We concluded that in healthy men HBO caused oxidative stress, which could not be prevented by dietary vitamin C plus E supplementation. The present data support the idea that HBO is a suitable model for oxidative stress in healthy volunteers.

Previous cross-sectional studies have shown that sedentary males, unlike their active counterparts, are unable to compensate for previous energy intake (EI). The present study therefore investigated the effects of a 6-week moderate exercise programme (4 times per week, 65–75 % maximal heart rate) on appetite regulation in healthy sedentary volunteers using a longitudinal design. EI at a buffet meal 60 min after high-energy (HEP; 607 kcal) and low-energy (LEP; 246 kcal) preloads, together with 24 h cumulative EI, were measured in twenty-five healthy volunteers (eleven men; mean age 30 (SD 12) years, mean BMI 22·7 (SD 2·3) kg/m2), at baseline and after the exercise intervention. Subjective hunger and fullness were assessed throughout using visual analogue scales. ANOVA showed a significant preload ×  exercise interaction on 24 h cumulative EI, supporting an improvement in appetite control over this time period with the exercise programme. There was a trend towards improvement in energy compensation over the same period (8·9 (SD 118·5) % v. 79·5 (SD 146.·4) %; P = 0·056). No preload ×  exercise interaction was observed for buffet EI. Secondary analysis, however, showed that although buffet EI after the two preloads was not significantly different at baseline, buffet EI after the HEP was significantly lower than after the LEP following the exercise intervention. The improvement in short-term appetite control with exercise was not explained by changes in subjective hunger or satiety. This longitudinal study supports the original cross-sectional findings and suggests that exercise may have a significant impact on short-term appetite control by leading to a more sensitive eating behaviour in response to previous EI. Further studies are needed to clarify the mechanisms involved.

Obesity is generally associated with high intake of junk foods rich in energy, fat, sugar and salt combined with a dysfunctional control of appetite and lack of exercise. There is some evidence to suggest that appetite and body mass can be influenced by maternal food intake during the fetal and suckling life of an individual. However, the influence of a maternal junk food diet during pregnancy and lactation on the feeding behaviour and weight gain of the offspring remains largely uncharacterised. In this study, six groups of rats were fed either rodent chow alone or with a junk food diet during gestation, lactation and/or post-weaning. The daily food intakes and body mass were measured in forty-two pregnant and lactating mothers as well as in 216 offspring from weaning up to 10 weeks of age. Results showed that 10 week-old rats born to mothers fed the junk food diet during gestation and lactation developed an exacerbated preference for fatty, sugary and salty foods at the expense of protein-rich foods when compared with offspring fed a balanced chow diet prior to weaning or during lactation alone. Male and female offspring exposed to the junk food diet throughout the study also exhibited increased body weight and BMI compared with all other offspring. This study shows that a maternal junk food diet during pregnancy and lactation may be an important contributing factor in the development of obesity.

Our aim was to determine whether short-term weight loss on a low-carbohydrate/low-saturated fat diet improved endothelial function compared with a conventional high-carbohydrate diet, as this diet is expected to lower both blood glucose and LDL-cholesterol. In a randomised parallel design of two energy-restricted diets in an outpatient setting, thirty-six subjects (BMI 33 (sem 4) kg/m2) were randomised to a low- or high-carbohydrate diet both low in saturated fat. Flow-mediated dilatation (FMD), fasting glucose, insulin, lipids, adiponectin and adhesion molecules were measured at baseline, during weight loss and at 52 weeks. FMD did not change with either diet (5·2 (sem 0·6) to 5·5 (sem 0·6) %) despite weight loss of 5 % and significant reductions in glucose and insulin and LDL-cholesterol and was not different after sustained weight loss of 5 % at 52 weeks. Adiponectin fell by 6 % at 12 weeks (P = 0·1) with weight loss but rose by 17 % at 12 months (P < 0·05) with 5 % weight loss. There were no effects of diet. In contradistinction, adhesion molecules fell at 12 weeks, vascular cell adhesion molecule-1 by 14 % and intracellular adhesion molecule-1 by 13 % (both P < 0·05). There were correlations between change in adiponectin at 12 months and change in HDL (r 0·778, P < 0·01) and glucose (r − 0·563, P = 0·057). In summary, weight loss does not improve FMD. Novel cardiovascular risk factors improved at 12 weeks but the improvement in adiponectin was delayed.

The effects of conjugated linoleic acid (CLA) on body weight and body composition in man are controversial. The aim of this study was to investigate the effects of milk supplementation with CLA on body composition and on the biochemical parameters of the metabolic syndrome. This was a randomised, double-blind, placebo-controlled trial. Subjects were randomised to a daily intake of 500 ml milk supplemented with 3 g CLA (using a mixture of the bioactive isomers cis-9, trans-11 and trans-10, cis-12, marketed as Tonalin®, Naturlinea; Central Lechera Asturiana) or placebo for 12 weeks. Sixty healthy men and women (aged 35–65 years) with signs of the metabolic syndrome participated (BMI 25–35 kg/m2). Dual-energy X-ray absorptiometry was used to measure body composition (week 0 baseline and week 12). Total fat mass in the CLA-milk subgroup with a BMI ≤ 30 kg/m2 decreased significantly while no changes were detected in the placebo group (~2 %, P = 0·01). Trunk fat mass showed a trend towards reduction (~3 %, P = 0·05). CLA supplementation had no significant effect on the parameters of the metabolic syndrome, nor was it associated with changes in haematological parameters or renal function. The supplementation of milk with 3 g CLA over 12 weeks results in a significant reduction of fat mass in overweight but not in obese subjects. CLA supplementation was not associated with any adverse effects or biological changes.