No description available.

<p> Depression is a leading cause of disability and mortality worldwide, especially for women. No nutrition recommendations exist for depression. Oral contraceptives (OCs) have become the leading form of pregnancy prevention in the United States. Studies have associated OC use with impaired nutrient status, specifically folate, vitamin B₁₂, and vitamin B₆, which also affect brain functions. Dietary folate, vitamin B12, and vitamin B6 self-reported intakes were used to determine the relationship between depression in women who used OCs (<i>n</i> = 34) in a selected cohort (<i> n</i> = 409) from the National Health and Nutrition Examination Survey, 2003&ndash;2008. OC users were more depressed than non-OC users; depression was associated with various quartile levels of vitamin intake (<i>p</i> &lt;.001). No benefit was observed with intakes which exceeded RDAs for non-OC users; OC users were less depressed when intakes exceeded RDAs for folate, vitamin B₁₂, and vitamin B6 by 13%, 75%, and 7%, respectively. </p>

<p> Non-alcoholic fatty liver disease (NAFLD) has become the leading cause of chronic liver disease. The spectrum of NAFLD ranges from simple steatosis, to non-alcoholic steatohepatitis (NASH), fibrosis, cirrhosis, and potentially hepatocellular carcinoma. Dietary factors and chemical exposure have been associated with the disease progression. In addition, the presence of NAFLD changes the metabolism of drugs and chemicals, which may in turn increase the susceptibility of the liver to xenobiotic induced toxicity. To examine the potential interplay of chemicals on diet-induced NAFLD, three studies were conducted in this dissertation project. In the first study, a mouse model was established that recapitulated the spectrum of liver damages seen in human NAFLD. Using a high fat diet (HFD), steatosis, NASH, progressive fibrosis, and liver tumor formation were produced in mice. Modulations of nuclear receptors involved in metabolism of endogenous and xenobiotic compounds were characterized at various stages of NAFLD. Using this mouse model, a second study examined if perfluorooctanoate (PFOA), a ubiquitous environmental contaminant, modulated the progression of NASH. The results showed PFOA induced hepatic DNA synthesis and liver inflammation were exacerbated in the mice fed with HFD. In contrast, PFOA decreased the severity of hepatic steatosis and fibrosis induced by HFD. To further investigate the mechanisms underlying these observed effects, a third study was performed that analyzed the hepatic transcriptome in liver samples taken from studies 1 and 2. The results of the third study demonstrated that cytokine and chemokine-related genes played important role in the development of both inflammation and fibrosis in NAFLD. Comparing PFOA to vehicle controls in HFD fed mice, PFOA disrupted the lipid homeostasis to favor clearance in the fatty liver, as most of the genes were enriched in the fatty acid oxidation pathways. In summary, this project established and a mouse model of HFD induced NAFLD and characterized the interplay of diet and chemicals in the disease progression. The results from this dissertation also indicated that patients with NAFLD may respond differently compared with healthy individuals. The potential susceptibility of this population to chemically induced hepatotoxicity needs to be carefully considered when assessing risk.</p><p>

There are no practical options to reduce breast cancer risk in American women that are without side-effects. Almost all preventive strategies are designed to diminish the role of estrogens in promoting breast cell proliferation. Brassica vegetables (e.g., broccoli) contain indole glucosinolates that can shift estrogen metabolism away from the highly estrogenic 16α-hydroxyestrone (16HE) and toward 2-hydroxyestrone (2HE), which has little estrogenic activity on breast cells. The relative strength of these two pathways is measured in urine as the ratio 2HE/16HE (2/16). In controlled trials that have enrolled premenopausal women or young men, large quantities of Brassica vegetables or indole glucosinolate derivatives decreased urinary 16HE levels relative to 2HE levels, possibly lowering breast cancer risk. However, in order to be an acceptable and effective preventative, Brassica vegetables must shift estrogen metabolism as Brassica consumption is practiced within free-living women. The goal of this research is to determine if Brassica should be further explored as a strategy to prevent breast cancer. In order to do so, it was determined that three issues must be addressed: (1) Brassica consumption must increase the 2/16 ratio among healthy free-living women, without serious side-affects, (2) the 2/16 ratio must be a valid indicator of breast cancer risk, and (3) a reliable and valid method to estimate Brassica consumption must be identified. As part of this research, thirty-seven healthy postmenopausal women participated in a dietary intervention designed to facilitate daily Brassica consumption. The diet, 2/16, and other information were measured before, during, and after the intervention. The 2/16 ratio significantly increased with greater Brassica intake. However, urinary 2/16 levels between participants were sensitive to dietary fat and fiber intake, and future studies evaluating the 2/16-breast cancer association should control for macronutrient intake. Dithiocarbamate excretion, a biomarker of Brassica consumption, inconsistently predicted self-reported Brassica intake and is sensitive to the types of vegetables consumed. However, DTC may be useful to rank-order participants in epidemiological studies. Overall, to the extent that lower 2/16 values are associated with increased breast cancer risk, Brassica vegetables may be an important component of any strategy to reduce breast cancer risk.

Thesis (Ph. D.)--Washington State University, December 2009. / Title from PDF title page (viewed on Dec. 16, 2009). "School of Economic Sciences." Includes bibliographical references.

Thesis (PH.D.)--Syracuse University, 2003. / "Publication number AAT 3113236."

This thesis describes the development of the idea of an 'obesity epidemic' that figures prominently in contemporary public health discourse. It uses conceptual approaches from Science and Technology Studies and the history of medicine to analyse changing ideas about obesity, particularly as formulated and mobilised by British researchers from the 1960s onwards, to show how excess body weight became understood as a significant public health problem in this period. The thesis begins by describing the post-war refocusing of medical attention in developed countries from infectious diseases, the rates of which are falling, to chronic disease such as heart disease, diabetes, cancer and stroke. Heart disease, in particular, became seen as an 'epidemic'. After World War II, increase research funding by the American government made possible the development of a new research method - the long-term prospective epidemiological study - and a new way of understanding chronic diseases as caused by risk factors such as high blood pressure, cigarette smoking and high blood cholesterol. Excess body weight was includes in this list of risk factors, and so became an object in increased medical attention. The thesis then outlines how a new public health coalition was formed around obesity in the 1970s by British biomedical researchers working on topics in the fields of nutrition, diabetes and coronary heart disease. It describes the development of what I call the 'individual paradigm' of obesity which characterises the condition as an individual problem that leads to heart disease and mechanical complaints and is treatable by weight loss diets. It then describes two key features of British obesity science in the 1980s and 1990s. The first of these is the adoption of the Body Mass Index and the standard cut-off points that are used to define overweight and obesity, which together facilitate the collection and dissemination of data on changes in average body weights, The second is the energy balance model of weight regulation, which served to unify the diverse disciplinary approaches to biomedical research incorporated into this new knowledge, but which could not account for the high rates of failure acknowledged as occurring with conventional treatments such as weight loss diets, anorectic drugs and bariatric surgery. The thesis describes how researchers in the field of obesity science than extended their institutional research to participate in the production of a series of reports for the World Health Organization, including one on the global epidemic of obesity published in 2000. This new platform, combined with data produced by prospective studies, enabled them to disseminate a new understanding of obesity and overweight - what I call the 'environmental paradigm' - which characterises it as a global health problem associated with an increased risk of many diseases and caused by structural factors such as inappropriate diet and sedentary lifestyles. Despite refocusing attention of structural determinants of ill health, however, public health experts were constrained by considerations of political practicality and commercial interest when calling for preventive measures in the areas of diet and physical activity. The thesis concludes by considering the different ways in which scholars have theorised the epidemiological transition from infectious to chronic disease. Drawing on approaches from the health inequalities literature, it argues that the conventional framings of chronic disease epidemiology have tended systematically to obscure structural links between obesity and other forms of diet-related ill health on the one hand, and relative poverty on the other.

Thesis (Ph. D.)--University of Adelaide, 2001. / Title from PDF title page (viewed on May 1, 2005). Includes bibliographical references (p. 327-346).

This thesis presents five standalone essays that demonstrate the feasibility and utility of employing advanced analytic techniques to cross-sectional data from Indonesia in order to deal with some technical challenges typically encountered either in the estimation of social gradient in health or in the monitoring and evaluation of well-being as a multidimensional construct. The first essay estimates the causal effect of poverty on mental health by exploiting a natural experiment induced by weather variability across 440 districts in the Indonesian archipelago. The second essay applies parametric anchoring vignette methodology to investigate the extent to which the estimates of demographic and socio-economic inequalities in self-rated health are biased by survey respondents' differential reporting behaviour. The third essay formally assesses the existence and identifies the social determinants of the double burden of malnutrition in Indonesia using a variant of a generalised linear mixed model. The fourth essay maps the social and spatial distributions of malaria in 27 districts in Indonesian Papua using a probabilistic disease mapping technique that is capable of accounting for the complex dependency structure of spatially-correlated multilevel data. The fifth essay examines the extent and patterns of multidimensional poverty in Indonesia over the last decade using a novel poverty measurement method that is sensitive to both the incidence and intensity of multiple deprivations in income, health and education domains. Together, these essays show that although health and social researchers in the developing world have little choice but to conduct cross-sectional studies, new insights can sometimes be gained if one is willing to look at existing data through a new lens. In all five cases presented here, this approach is proved to be useful in shaping practical policy-making.

Doctor of Philosophy / Human Nutrition / Richard R. Rosenkranz / Child stunting refers to a condition where the child is relatively shorter in height, in comparison to their age group. Child stunting is a public health nutrition problem that hinders the development of future generations, not only physiologically but also potentially deprives their cognitive function and productivity. The demographic transition, conjoined with the epidemiological and nutrition transitions, has resulted in the coexistence of an over- and under-nutrition problem known as double burden of malnutrition, and child stunting has been a persistent part of the problem. In 2014, the World Health Organization (WHO) reported that one-fourth of the children in the developing countries have been suffering from child stunting. The objective of this research was to apply the behavioral epidemiology approach to tackle child stunting in households with double burden of malnutrition. It was hypothesized that unlike any other households with problem of child stunting, households with double burden of malnutrition possess some degree of capacity that, with proper support and direction, might enable them to help themselves reduce or prevent this nutrition-related debacle. Results from a secondary data analysis revealed that child stunting was associated with lower dietary diversity as an indication of poor food choice in the household, related to children’s nutrient requirements. Another cross-sectional study in this dissertation was conducted in an urban setting in Indonesia, and found that households with child stunting alone was associated with extreme food insecurity, while households with double burden of malnutrition ─ in the form of stunted child and overweight/obese mother (SCOWT) ─ was associated with even a mild degree of food insecurity. These results support our hypothesis that households with double burden of malnutrition lack the capacity to direct their resources properly to prevent child stunting. Most notably, we expected that the role of the mothers to manage healthy food choices through indirect measure of dietary diversity, availability and distribution within the household was lacking. In order to equip mothers with necessary components to be able to overcome these problems, we conducted a behaviorally based intervention that targeted mothers in the households experiencing the problem of double burden of malnutrition. The intervention provided the potential to achieve participant self-administered goal setting to improve diet, as well as child feeding behavior, by means of improved self-efficacy, nutrition literacy and dietary diversity. Maternal self-efficacy may be potentially enhanced by vicarious experience and active mastery experience gained during 6 sessions of behavioral intervention and verbal motivation by community health workers during 6 additional home visits. These studies, collectively comprising the present dissertation, present a message for policy makers in developing countries: nutrition literacy and behaviors for choosing healthy foods are lacking in mothers that affect both maternal and child food intake, but efforts such as improving vicarious and mastery experience on child feeding practices and healthy food choices can boost mother’s self-efficacy to engage in appropriate behaviors and improve their child’s nutrition.