Facilitators and barriers to the use of economic evaluations in nutrition and public health

Aims: Interventions targeting diets have the potential to reduce a consistent fraction of the chronic disease burden. Economic evaluations of such interventions can be an important tool in guiding public health practitioners and decision makers at various levels, yet there are still not many economic evaluations in this area. This qualitative study explored facilitators and barriers in conducting and using economic analyses to inform decision makers in the field of public health nutrition. Methods: Data were collected through written, open-ended questionnaires administered to twenty-three participants (13 from academia and 10 from government) using purposive sampling and analysed through a conventional content analysis. Results: The analysis revealed two broad categories of barriers, which included: i) “Methodological challenges”, and; ii) “Barriers related to application of economic evaluations.” Two main categories of facilitators were also identified: i) “Facilitators to improving the methodology of economic evaluations”, with subcategories further detailing frameworks and methods to be applied, and; ii) “Facilitators to broaden the use of economic evaluations”, with most subcategories addressing science-into-policy translations. These barriers and facilitators to the use of economic evaluations in public health are perceived differently by researchers and policymakers, the former more focused on implementation aspects, the latter more concerned by methodological gaps. Conclusion: Public health nutrition policies seldom take into account data from formal economic evaluations. Economic evaluation methodologies can be improved to ensure their broader application to decision making.   Conflicts of interest: None declared.   Acknowledgements: The work of AL is partially supported by a Jean Monnet Erasmus+ grant (574376-EPP-1-2016-1-IT-EPPJMO-MODULE)

Severe Atherosclerosis and Hypercholesterolemia in Mice Lacking Both the Melanocortin Type 4 Receptor and Low Density Lipoprotein Receptor

Dysfunction of the melanocortin system can result in severe obesity accompanied with dyslipidemia and symptoms of the metabolic syndrome but the effect on vascular atherogenesis is not known. To study the impact of obesity and dyslipidemia on the cardiovascular system, we generated mice double-deficient for the melanocortin type 4 receptor (Mc4r(mut) mice) and the LDL receptor (Ldlr(-/-) mice). Mc4r(mut) mice develop obesity due to hyperphagia. Double-mutant mice (Mc4r(mut);Ldlr(-/-)) exhibited massive increases in body weight, plasma cholesterol and triacylglycerol levels and developed atherosclerosis. Atherosclerotic lesion size was affected throughout the aortic root and brachiocephalic artery not only under semisynthetic, cholesterol-containing diet but also under cholesterol-free standard chow. The Mc4r(mut) mice developed a hepatic steatosis which contributes to increased plasma cholesterol levels even under cholesterol-free standard chow. Transcripts of cholesterol biosynthesis components and liver cholesterol levels did not significantly differ between wild-type and all mutant mouse strains but RNA sequencing data and biochemical measurements point to an altered bile acid elimination in Mc4r(mut);Ldlr(-/-). Therefore, the unchanged endogenous cholesterol biosynthesis together with a reduced hepatic VLDL and LDL-cholesterol clearance most likely led to increased plasma lipid levels and consequently to atherosclerosis in this animal model. Our data indicate that dysfunction of the melanocortin-regulated food intake and the resulting obesity significantly add to the proatherogenic lipoprotein profile caused by LDL receptor deficiency and, therefore, can be regarded as relevant risk factor for atherosclerosis

Facilitators and barriers to the use of economic evaluations in nutrition and public health

Abstract Aims: Interventions targeting diets have the potential to reduce a consistent fraction of the chronic disease burden. Economic evaluations of such interventions can be an important tool in guiding public health practitioners and decision makers at various levels, yet there are still not many economic evaluations in this area. This qualitative study explored facilitators and barriers in conducting and using economic analyses to inform decision makers in the field of public health nutrition. Methods: Data were collected through written, open-ended questionnaires administered to twenty-three participants (13 from academia and 10 from government) using purposive sampling and analysed through a conventional content analysis. Results: The analysis revealed two broad categories of barriers, which included: 1) “Methodological challenges,” and 2) “Barriers related to application of economic evaluations.” Two main categories of facilitators were also identified: 1) “Facilitators to improving the methodology of economic evaluations”, with subcategories further detailing frameworks and methods to be applied, and 2): “Facilitators to broaden the use of economic evaluations”, with most subcategories addressing science-into-policy translations. These barriers and facilitators are perceived differently by researchers and policymakers, the former more concerned by methodological gaps and the latter more focused on implementation gaps. Conclusion: Public health nutrition policies seldom take into account data from formal economic evaluations. Economic evaluation methodologies can be improved to ensure a their broader application to decision making.JRC.F.1-Health in Societ

Food-Based Dietary Guidelines database

Overview of European food-based dietary guidelines for the healthy adult population, validated by Member States.JRC.F.1-Health in Societ

Transcriptional changes of selected components of the cholesterol and bile acid biosyntheses.

<p>RNA sequencing was performed with RNA from livers of 10 animals of each genotype. Means of the expression ratio (KO/WT) for each gene are listed. For p-value calculations an unpaired two-tailed Student’s t-test was used.</p

Severe hypercholesterolemia and hypertriglyceridemia in mice lacking both MC4 and LDL receptors.

<p>Serum cholesterol (<b>A</b>) and serum triglycerides (<b>B</b>) were determined in the indicated mouse strains (n = 10–14 male mice). Female mice show essentially similar results (see <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0167888#pone.0167888.t002" target="_blank">Table 2</a>). The statistic evaluation is given in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0167888#pone.0167888.t002" target="_blank">Table 2</a>.</p

Blood glucose, serum urea levels, and liver enzymes on standard chow and semisynthetic diets.

<p>Enzyme activities of the different genotypes were determined after 184 ± 3 days after birth. Animals were kept on standard chow and semisynthetic diet. Data are given as means ± SD and tested for significance to the respective <i>Mc4r</i>^+/+: * p < 0.05, ** p < 0.01; *** p < 0.001. The number of animals/group is between 10 and 14.</p

Atherosclerosis in the aortic root in mice lacking Ldlr and Mc4r;Ldlr.

<p>Representative sections of the aortic root prepared from the different mouse strains. Depicted are sections of the aortic root of female and male <i>Mc4r</i>^<i>mut</i> and <i>Mc4r</i>^<i>mut</i>;<i>Ldlr</i>^-/- mouse strains fed a chow and semisynthetic diet (0.02% cholesterol).</p

Correlation between plasma cholesterol levels and plaque sizes of atherosclerotic lesions at the aortic root and brachiocephalic artery (BCA).

<p>Correlations were performed with the data of <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0167888#pone.0167888.t002" target="_blank">Table 2</a> and <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0167888#pone.0167888.g003" target="_blank">Fig 3</a>. To illustrate the results of the multiple regression analysis (see <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0167888#sec002" target="_blank">Material and Methods</a>), we plotted the cholesterol levels against the plaque size for males and females. Furthermore, we added a linear regression line computed separately for <i>Ldlr</i>^<i>-/-</i> with and without <i>Mc4r</i>^<i>mut</i> (regression coefficients are given in the figure, the respective p-values can be found in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0167888#pone.0167888.s003" target="_blank">S2 Table</a>).</p