There is a consensus that interventions to prevent and treat childhood obesity should involve the family; however, the extent of the child's involvement has received little attention. The goal of the present study was to evaluate the relative efficacy of treating childhood obesity via a family-based health-centred intervention, targeting parents alone v. parents and obese children together. Thirty-two families with obese children of 6–11 years of age were randomised into groups, in which participants were provided for 6 months a comprehensive educational and behavioural programme for a healthy lifestyle. These groups differed in their main agent of change: parents-only v. the parents and the obese child. In both groups, parents were encouraged to foster authoritative parenting styles (parents are both firm and supportive; assume a leadership role in the environmental change with appropriate granting of child's autonomy). Only the intervention aimed at parents-only resulted in a significant reduction in the percentage overweight at the end of the programme (P=0·02) as well as at the 1-year follow-up meeting.The differences between groups at both times were significant (P<0·05). A greater reduction in food stimuli in the home (P<0·05) was noted in the parents-only group. In both groups, the parents' weight status did not change. Regression analysis shows that the level of attendance in sessions explained 28% of the variability in the children's weight status change, the treatment group explained another 10%, and the improvement in the obesogenic load explained 11% of the variability. These results suggest that omittingthe obese child from active participation in the health-centred programme may be beneficial for weight loss and for the promotion of a healthy lifestyle among obese children.

The present study reports the activities of quercetin and its main circulating conjugates in man (quercetin-3′-sulphate (Q3′S) and quercetin-3-glucuronide (Q3G)) on in vivo angiogenesis induced by vascular endothelial growth factor (VEGF) and examines the effects of these molecules on cultured endothelial cells. We found opposing effects of quercetin and its metabolites on angiogenesis. While quercetin and Q3G inhibited VEGF-induced endothelial cell functions and angiogenesis, Q3′S per se promoted endothelial cell proliferation and angiogenesis. The inhibitory effect elicited by Q3G was linked to inhibition of extracellular signal-regulated kinases 1/2 (ERK1/2) phosphorylation elicited by VEGF. The activation of endothelial cells by Q3′S was associated to stimulation of VEGF receptor-2 and to downstream signalling activation (phosphatidylinositol-3 kinase/Akt and nitric oxide synthase pathways), ultimately responsible for ERK1/2 phosphorylation. These data indicate that the effects of circulating quercetin conjugates on angiogenesis are different depending on the nature of the conjugate. Q3G andQ3′S are the two major conjugates in plasma, but their ratio is dependenton several factors, so thatinhibition or activation of angiogenesis could be subtly shifted as a result of metabolismin vivo.

As part of its work on setting standards and establishing guidelines for nutrigenomics research, the European Nutrigenomics Organisation (NuGO) is developing bioethical guidelines for those engaged in human nutrigenomics studies. A NuGO working group developed a set of draft guidelines addressing four areas: (1) information and consenting prior to a nutrigenomicsstudy; (2) the generation and use of genotype information; (3) the establishment and maintenance of biobanks; (4) the exchange of samples and data. NuGO convened a workshop with a panel of invited external experts to assess the draft guidelines. The panel of experts confirmedthat these areas are important and that the development of specific bioethical guidelines for nutrigenomics research would therefore enhance the application of established international guidelines in this field of biomedical research.