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This thesis investigates the use of scientific evidence in the process of making public health policy. A case study located within a food regulation setting is used. The aim is to test theory against this case study. The outcome is a theoretical understanding of the use of scientific evidence in the policy-making process in a food regulation setting. Food regulation can influence food composition and food labelling and thereby affect the population's dietary intake. Frequently there are contested values, beliefs, ideologies and interests among stakeholders regarding the use of food regulation as a policy instrument to effect public health outcomes. The protection of public health and safety, taking into account evidence based practice, is generally employed by food regulators as the priority objective during the policy-making process to adjudicate among the competing expectations of stakeholders. However, this policy objective has not been clearly defined and is vulnerable to interpretation and application. The process by which folate fortification policy was made in Australia, in response to epidemiological evidence of a relationship between folate intake during the periconceptional period and reduced risk of neural tube defects, was analysed as a case study of the policy-making process. The folate fortification policy created a precedent for both food fortification and subsequently health claims policy in Australia. A social constructivist method was used to analyse the case study. The method involved deconstructing the food regulatory system into three levels; decision-making process; procedural; and political environment. Data aligned with each level of analysis was collected from 22 key informant interviews, documentary sources, field notes and surveys of both a random sample of the Australian population's knowledge of folate and use of folic acid-containing supplements (n = 5422), and the implementation of folate fortified food products into stores (n = 60). The insights that emerged from each of the three levels of analysis were assessed iteratively to identify a pattern of interrelationships associated with the policy-making process within the food regulatory system. The identified pattern was interpreted against existing theory to gain a theoretical understanding of the public health policy-making process in this political setting. The central argument of this thesis extends Sabatier and Jenkins-Smith's Advocacy Coalition Framework theory to a food regulation setting. The argument is that within the contemporary political climates of neoliberalism and globalisation, a coalition between corporate interests and the values of scientists with a positivist-reductionist approach to public health research is privileged so as to invoke certain scientific evidence to, in turn, legitimise food regulation policy decisions. The theory will help to inform policy-makers about how and why the public health policy objective in a food regulation setting is interpreted and applied. This will contribute to improving policy practice intended to effect public health outcomes. It is concluded that irrespective of the quantity and quality of the scientific evidence that is being made available, scientific evidence cannot be assumed to speak for itself Policy-making is an inherently political and value-laden process and the potential for politically motivated interpretation and application of otherwise value-neutral scientific evidence can undermine the investment in its generation. From this perspective, evidence based practice, far from liberating policy-making from political influence, can itself become part of the problem rather than the solution. Nevertheless, rational evidence based practice is an ideal to strive for and a series of recommendations is proposed to help make the use of evidence in current food regulation policy processes more transparent and democratic.

Thesis (Ph. D.)--University of Missouri-Columbia, 1998. / Typescript. Vita. Includes bibliographical references (leaves 141-152). Also available on the Internet.

Thesis (Ph. D.)--University of Missouri-Columbia, 1998. / Typescript. Vita. Includes bibliographical references (leaves 141-152). Also available on the Internet.

Thesis (Ph. D.)--University of Missouri-Columbia, 2002. / Typescript. Vita. Includes bibliographical references. Also available on the Internet.

Thesis (Ph. D.)--University of Missouri-Columbia, 2002. / Typescript. Vita. Includes bibliographical references. Also available on the Internet.

n-3 polyunsaturated fatty acids (n-3 PUFA) have been postulated to improve the insulin resistance associated with type 2 diabetes since the 1960s when observational studies in the Alaskan Inuit noted a reduced prevalence of type 2 diabetes when this population consumed a traditional diet. These findings were supported by animal studies but results of human intervention studies have been variable with most showing no change in glucose metabolism. More recent studies in growing farm animals suggested that muscle membrane phospholipids required to be enriched to a minimum of 14% n-3 PUFA in order for a change in insulin sensitivity to occur. This study sought to establish the effect of long-term (9 month) high-dose (3g/day) supplement of the n-3 PUFA eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) on insulin sensitivity of glucose and protein metabolism. Thirty-three subjects with impaired glucose regulation underwent hyperinsulinaemic-euglycaemic-euaminoacidaemic clamps pre- and postintervention of n-3 PUFA or a control (maize) oil. A second cohort who all received n-3 PUFA supplementation underwent pre- and post-intervention muscle biopsies. Secondary outcomes included an assessment of inflammatory status and determining whether erythrocyte membrane phospholipid could act as a surrogate for muscle membrane phospholipid. In the clamp cohort, there were no changes in glucose metabolism postintervention; however, there was an increase in insulin-stimulated protein metabolism following the fish oil intervention. In the biopsy cohort, no subject achieved 14% PUFA enrichment in muscle membrane phospholipids; however, all subjects who received n-3 PUFA supplementation did achieve a minimum of 14% enrichment of n-3 PUFA in erythrocyte membrane phospholipid. In agreement with the majority of the literature, n-3 PUFA did not affect glucose metabolism. Insulin-stimulated protein metabolism was improved supporting the findings of another recent human study. These changes in protein metabolism may reduce the sarcopenia associated with aging, potentially delaying the progression of frailty.

Exposure to methyl mercury (MeHg) is a global concern. Increased chronic exposure to MeHg among fish and marine mammal consuming populations will increase the risk of prenatal exposure and as a result, the risk of infant brain damage and neurotoxcity. It is therefore important to understand the role of environmental factors, such as nutrition, in determining susceptibility to MeHg toxicity. Three nutrients (selenium (Se), vitamin C and vitamin E) were selected for examination of their interactions with the mechanisms of McHg cytotoxicity in vitro. Two hybrid neural cell lines (M03.13 and NSC-34) were evaluated for their usefulness in the study of MeHg cytotoxicity. Sixteen toxic endpoints were selected for investigation of growth, viability, structure and biochemistry. Both cell lines responded to MeHg exposure in a dose dependent manner for the majority of endpoints suggesting that both MO3.13 and NSC-34 cells undergo structural and biochemical changes during exposure to McHg, but that MO3.13 cells are more sensitive to DNA, mitochondria) membrane damage and glutathione (GSH) depletion and that NSC-34 cells are more sensitive to protein damage and apoptosis. Se exposure lessened the MeHg-induced decrease in DNA and GSH concentrations in both cell lines. In NSC-34 cells, Se also increased F-actin concentrations and prevented an increase in caspase-3 activity. Se may alter the mechanism of cell death by preventing McHg disruption of DNA replication thus maintaining the production and function of peptides (GSH) and protein (polymerized actin) that aid in MeHg detoxification and neural function. In NSC-34 cells, vitamin C prevented the induction of caspase-3 activity and lessened DNA damage and GSH depletion. Vitamin E lessened GSH depletion and lessened G-actin depletion. Both vitamin C and E improved GSH status, but vitamin C also delayed McHg damage of DNA and prevented early signs of apoptosis suggesting these two vitamins interfere with MeHg metabolism by diffe

Lifestyle and dietary predictors of total fat intake (%kcal) were examined, to identify groups potentially at risk of hypercholesterolemia. In 1987, 301 Montreal adults were sampled by random digit dialing. A diet history and lifestyle habits were recorded. Mean total fat intake (%kcal) was 34.75% ($ pm$6.23). Principal Components Analysis identified specific dietary patterns. Regression analyses indicated that the first 4 food factors were associated with total fat intake (%kcal p $<$ 0.01). Household size was inversely related to total fat (%kcal); 0.8% less kcal from fat for each additional member of the household (p $<$ 0.01). Females had 2.8% more kcal from fat than males (p $<$ 0.01). The number of fast food meals consumed per week was positively associated with outcome when age was considered (p $<$ 0.05). BMI and education level were not associated with total fat (%kcal). Smoking was associated with intake of higher fat foods (p $<$ 0.01). These predictors can identify groups in the population who may be at increased cardiovascular risk.

To examine the effects of fat composition and supplemental vitamin E (Vit E) and selenium (Se) on in vivo lipid peroxidation, diet-induced hypercholesterolemia, and glutathione (GSH) metabolism, male Syrian hamsters were fed for three weeks butter fat (BF-) or fish oil- (FO-)based diets supplemented with Vit E and/or Se. The effect of supplemental Vit E and Se on tissue lipid peroxidation (LPO), glutathione peroxidase (GSH-Px) activity and GSH concentrations differed between heart and liver and also was affected by dietary fat. The reduced glutathione/oxidized glutathione (GSH/GSSG) ratio was more consistently associated with tissue lipid peroxidation than was tissue Vit E content. Plasma lipids were lowered with supplemental Se and Vit E. Se supplementation, however, exerted a more potent hypolipidemic effect than Vit E. A pro-oxidative action of Se in hearts of FO-fed hamsters was noted, which was inhibited by supplemental Vit E. Hence, the combination of Vit E and Se may offer the most benefit against diet-induced oxidative stress and hyperlipidemia.