The creative turn in evidence for public health: community and arts-based methodologies.

Background: We propose that arts based methodologies can be of value in the production and exchange of evidence in supporting public health related policy. This article reports on a collaborative piece of work resulting from two projects which took place in a former coal mining town in South Wales. Methods: We used a participatory framework whereby researchers, community members and artists co-produced 'evidence' through the creative arts to inform public policy. We collected a range of data using a number of different techniques, including interviews, focus groups and observation, but also included an extensive range of creative activities. Results: The data provided a diverse range of perspectives on how people of different ages live their lives. The People's Platform was a performance-based debate which was the culmination of the collaboration. The show involved a series of short performances with time for facilitated discussion in-between. It was felt that the show facilitated knowledge exchange on health and wellbeing issues that are usually difficult to express and understand through traditional forms of evidence. Conclusion: Whilst arts-based approaches are not free from risk, they offer an alternative form of knowledge as a necessary complement to the range of data available to policy makers.

Inactivation of Ppp1r15a minimises weight gain and insulin resistance during caloric excess in female mice.

Phosphorylation of the translation initiation factor eIF2α within the mediobasal hypothalamus is known to suppress food intake, but the role of the eIF2α phosphatases in regulating body weight is poorly understood. Mice deficient in active PPP1R15A, a stress-inducible eIF2α phosphatase, are healthy and more resistant to endoplasmic reticulum stress than wild type controls. We report that when female Ppp1r15a mutant mice are fed a high fat diet they gain less weight than wild type littermates owing to reduced food intake. This results in healthy leaner Ppp1r15a mutant animals with reduced hepatic steatosis and improved insulin sensitivity, albeit with a possible modest defect in insulin secretion. By contrast, no weight differences are observed between wild type and Ppp1r15a deficient mice fed a standard diet. We conclude that female mice lacking the C-terminal PP1-binding domain of PPP1R15A show reduced dietary intake and preserved glucose tolerance. Our data indicate that this results in reduced weight gain and protection from diet-induced obesity.