Benchmarking government action for obesity prevention--an innovative advocacy strategy.

BACKGROUND: Successful obesity prevention will require a leading role for governments, but internationally they have been slow to act. League tables of benchmark indicators of action can be a valuable advocacy and evaluation tool. OBJECTIVE: To develop a benchmarking tool for government action on obesity prevention, implement it across Australian jurisdictions and to publicly award the best and worst performers. DESIGN: A framework was developed which encompassed nine domains, reflecting best practice government action on obesity prevention: whole-of-government approaches; marketing restrictions; access to affordable, healthy food; school food and physical activity; food in public facilities; urban design and transport; leisure and local environments; health services, and; social marketing. A scoring system was used by non-government key informants to rate the performance of their government. National rankings were generated and the results were communicated to all Premiers/Chief Ministers, the media and the national obesity research and practice community. RESULTS: Evaluation of the initial tool in 2010 showed it to be feasible to implement and able to discriminate the better and worse performing governments. Evaluation of the rubric in 2011 confirmed this to be a robust and useful method. In relation to government action, the best performing governments were those with whole-of-government approaches, had extended common initiatives and demonstrated innovation and strong political will. CONCLUSION: This new benchmarking tool, the Obesity Action Award, has enabled identification of leading government action on obesity prevention and the key characteristics associated with their success. We recommend this tool for other multi-state/country comparisons.

Rapid potentiation of endothelium-dependent vasodilation by estradiol in postmenopausal women is mediated via cyclooxygenase 2.

Estrogens influence cardiovascular function through direct and indirect effects and via genomic and nongenomic mechanisms. The pathways underlying the nongenomic mechanisms are not completely understood. Estrogen-induced responses in vascular cells have been shown to influence prostaglandins and cyclooxygenase (COX), a key enzyme in the production of prostaglandins, with two isoforms, COX-1 and COX-2. We investigated the effects of prostaglandins on the acute potentiation by 17beta-estradiol (E) of acetylcholine (ACh)-mediated vasodilation in the cutaneous vasculature. Using a double-blind placebo-controlled design, we assessed skin blood flow in 32 healthy, postmenopausal women by laser Doppler velocimetry with direct current iontophoresis of ACh and sodium nitroprusside before and after 6-wk treatment periods with aspirin (a nonspecific COX-1 and COX-2 inhibitor), diclofenac (predominantly a COX-2 inhibitor, which also inhibits COX-1), celecoxib (a specific COX-2 inhibitor), given at anti-inflammatory doses, or placebo. Blood flux values before iontophoresis of ACh did not differ between the treatment groups or after E administration, excluding a direct cutaneous vasodilator effect of the treatments or of E. Acute E administration enhanced the response to ACh after aspirin, diclofenac, and placebo; however, this effect was completely abolished with celecoxib treatment (P < 0.05). E had no effect on sodium nitroprusside-mediated vasodilation after any of the treatments. We conclude that the COX-2 pathway plays a specific role in the rapid E-induced potentiation of cholinergic vasodilation in postmenopausal women.