Doctor of Philosophy / Department of Plant Pathology / Karen A. Garrett / Late blight of potato, caused by Phytophthora infestans, is a pernicious disease of potatoes worldwide. This disease causes yield losses as a result of foliar and tuber damage. Many models exist to predict late blight risk for control purposes with-in season but rely upon fine-scale weather data collected in hourly, or finer, increments. This is a major constraint when working with disease prediction models for areas of the world where hourly weather data is not available or is unreliable. Weather or climate summary datasets are often available as monthly summaries. These provide a partial solution to this problem with global data at large time-steps (e.g., monthly). Difficulties arise when attempting to use these forms of data in small temporal scale models. My first objective was to develop new approaches for application of disease forecast models to coarser resolution weather data sets. I created metamodels based on daily and monthly weather values which adapt an existing potato late blight model for use with these coarser forms of data using generalized additive models. The daily and monthly weather metamodels have R-squared values of 0.62 and 0.78 respectively. These new models were used to map global late blight risk under current and climate change scenarios resistant and susceptible varieties. Changes in global disease risk for locations where wild potato species are indigenous, and disease risk for countries where chronic malnutrition is a problem were evaluated. Under the climate change scenario selected for use, A1B, future global late blight severity decreases. The risk patterns do not show major changes, areas of high risk remain high relative to areas of low risk with rather slight increases or decreases relative to previous years. Areas of higher wild potato species richness experience slightly increased blight risk, while areas of lower species richness experience a slight decline in risk.

Human population-based studies of longitudinal design observe that higher intelligence in youth confers protection from premature mortality in adulthood. This field of study (“cognitive epidemiology”; Deary & Batty, 2007) has firmly established associations between intelligence and health outcomes, and has begun to address the likely mechanisms involved. The present thesis assessed some social, educational, and lifestyle factors that potentially confound and/or mediate the intelligence-mortality link. First, I carried out a systematic review of longitudinal cohort studies reporting intelligence differences in youth in relation to adult mortality risk, and in meta-analysis I aggregated the effect sizes from 16. A one SD advantage in intelligence scores was associated with 24% (95% CI 23% to 25%) lower risk of death, during 17- to 69-year follow-up; this magnitude showed no sex differential. Socioeconomic status in early life did not explain the effect. Rather, the person’s own occupational status in adulthood and educational attainment explained a third and a half of the association, respectively. One issue in controlling for education, in such models, is its strong correlation with intelligence test performance, which could lead to statistical overadjustment. A second aspect of this thesis, therefore, addressed the nature of the intelligence-education covariance in two behaviour-genetic studies of large general population-based samples of schoolchildren from England and The Netherlands. Previous studies that reported intelligence—education genetic covariances were potentially biased in their use of twin self-selection or pre-selection sampling. Moreover, the analysis in this thesis used a novel statistical approach, and included non-twin data to represent fully the variance in performance scores of a population. Analysis of the English cohort confirmed the top end of estimates from previous studies: 76% to 88% of the phenotypic correlation was due to heritability. The Dutch cohort showed greater variance for equivalent estimates (33% to 100%). The results indicate a limit to the extent to which education and intelligence might be causative of one another suggesting caution in interpreting some of the substantive attenuation effects by education reported in the literature. Third, I investigated pathways from intelligence to cardiovascular disease risk factors, given the consistent and robust finding that an advantage in intelligence relates to lower cardiovascular disease-outcomes. I used data from the 1958 National Child Development Study to investigate age-11 intelligence in association with inflammatory and haemostatic biomarker status at age 46 years. The results replicated inverse associations previously reported in an older age sample, and a one SD advantage in intelligence related to a 1.1mg/L decrease in C-reactive protein. The effect was largely mediated by lifestyle factors, including smoking, occupational status and abdominal obesity. In two further studies I used the west of Scotland Twenty-07 cohort, to investigate processing speeds among 16, 36 and 56 year-olds in relation to: (1) Inflammation, and (2) metabolic-risk, after 20 years. The advantage of experimental rather than psychometric measures of cognitive ability is their reduced cultural and social bias. Faster reaction time predicted lower systemic inflammation in the youngest male cohort, which appeared to be partially confounded by baseline smoking and socioeconomic status. Furthermore, advantage in reaction time performance in the young and middle-aged cohorts significantly predicted reduced metabolic risk. This was partially explained by occupational status, but retained statistical significance in some fully-adjusted models. A one SD advantage in age 16 simple reaction time variability, related to the 21% (95% CI 12% to 30%) reduced odds of metabolic syndrome by age 36 in the basic model, and this effect remained unchanged after controlling for all covariates. The growing evidence for specific social and behavioural factors that mediate intelligence-to-mortality pathways are discussed, in respect of indirect evidence that underlying system integrity or early life confounding may contribute incrementally to the effect.

published_or_final_version / Community Medicine / Master / Master of Public Health

Prediction for future coronary artery disease (CAD) from high-density lipoprotein (HDL) and triglyceride (TG) measurements are based off of a single measurement that has been shown to be variable. To better determine risk for CAD based on blood lipids, studies in the postprandial state are warranted. To assess the reproducibility of TG clearance, 10 men underwent three trials of a 70g oral fat loading test with blood samples collected every two hours for eight hours. These trials were all scheduled at least one week apart. Men who had fasting TG concentrations > 250 mg - dL -' were excluded from the study. Each subject presented to the laboratory having abstained from exercise for 24 hours and alcohol 72 hours prior to the upcoming trial. Each subject was also provided with a standardized frozen dinner to eat the night before at a time which allowed the subject to be 12 hours fasted for the next days' trial. To specifically assess postprandial lipemia, TG concentrations were plotted against bi-hourly collection times to form a curve. The area under this curve was then calculated to determine PPL area. Itwas found that there was no significant difference in area under the TG curve (p = 0.25) for any of the three trials (1096 ± 168, 948 ± 105, and 995 ± 127 mg - dL -' - 8 • hr-' respectively for trials one, two, and three). Pearson correlations between trials were 0.79 for trials one and two, 0.82 for trials two and three, and 0.90 for trials one and three. Also, there was no significant difference in peak TG (p = 0.34) on each of the three trial days (167 ± 27, 150 ± 16, and 151 ± 19 mg • dL -1 in peak TG for trials one, two, and three respectively). Time taken to reach peak TG concentrations (p = 0.20) or time to return to baseline TG (p = 0.27) were not significantly different across three trial days. The men in this study reached peak TG concentrations in this study in 3.2 ± 0.5, 4.0 ± 0.4, 4.0 ± 0.3 hours respectively for trials one, two, and three. Time to return to baseline was 6.8 ± 0.6, 7.4 ± 0.4, 7.8 ± 0.4 hours for trials one through three respectively. Correlations between trials and the lack of a difference between trials using repeated measures ANOVA in regards to PPL area gives some preliminary evidence that some postprandial measures such as PPL area and can be reproduced across trials. However, the intra-individual variation was 19 ± 4% which provides no additional support for reproducibility of PPL. Additionally, results from this study, as well as all others pertaining to the study of reproducibility of PPL are specific to the protocol used and the method of interpretation. / School of Physical Education

The Health Belief Model was used to study HIV/AIDS beliefs of 419, 18 to 24 year old, never married, sexually active, heterosexual college students and predict their AIDS preventive behaviors from a larger sample of 662 college students. The structural properties of the scales used were evaluated using confirmatory factor analysis. Recent preventive behaviors were predicted in a LISREL Structural Equation Modeling analysis.

This dissertation breaks new ground. It examines the perceptions of older adults towards AIDS prevention. Using the National Health Interview Survey, 1988: AIDS Knowledge and Attitudes Supplement, a modified Health Belief Model is developed. Despite the low number of older adults 55+ with AIDS, some extenuating circumstances increase their risk of AIDS contraction. Older adults have lower levels of knowledge about AIDS, weaker immune systems and receive more blood transfusions. Societal influences include educational neglect at the hands of physicians, healthcare workers and social service personnel. The first stage of the dissertation involved establishing older adults as an at-risk population through an extensive literature review. Next, the data was described utilizing frequencies, correlations and factor analysis. Frequencies clearly indicated that older adults in the data set had low levels of AIDS knowledge and did not view themselves at risk for AIDS contraction. Correlations between the variables were minimal. A modified Health Belief Model was developed and tested. Multiple regression determined that minimal variation in the two dependent variables, "Perceived Effectiveness of Effective Methods to Prevent AIDS Contraction" and "Perceived Effectiveness of Ineffective Methods to Prevent AIDS Contraction" was accounted for by the independent variables. Although F ratios allowed rejection of the two null hypotheses, beta weights were low. Adjusted R^2's accounted for only 21% and 16% respectively of the variation in the dependent variables. Finally, discrepancies in the model were determined and recommendations made for further research. Most health belief models concentrate on individual social-psychological variables. Due to AIDS' societal consequences, it is proposed that societal providers of education: physicians, social service workers and healthcare personnel need to be included in the model. Recommendations were made for additional research into sexual behavior of older adults and exploration of available training of physicians, healthcare and social service professionals. Finally, recommendations were made to provide training and education for both professionals as well as the elderly to prevent their growth into an at-risk population.

De nombreux facteurs de risque cardiovasculaire comme l’hypercholestérolémie, l’hypertension, et le diabète sont comptés parmi les facteurs de risque modifiables les plus importants pour le déclin cognitif et la démence. L’exposition à ces facteurs de risque au cours de la vie en particulier avant l’âge de 65 ans ainsi que leur agrégation contribuent de manière plus importante au déclin cognitif. Peu d’études se sont intéressées aux mesures composites de risque cardiovasculaire par rapport à la fonction cognitive chez les sujets de moins de 65 ans. L’objectif de cette thèse était d’étudier l’association entre les mesures composites de risque et le déclin cognitif au cours de la phase précocedu vieillissement. Les données de la cohorte Whitehall II dans laquelle les fonctions cognitives ont été mesurées à trois reprises ont été utilisées pour étudier l’association entre le syndrome métabolique et deux scores de risque de Framingham (de maladie cardiovasculaire globale et d’AVC), et la fonction cognitive et le déclin cognitif sur 10 ans. Les scores de risque cardiovasculaire de Framingham ont aussi été comparés avec un score de risque de démence. De toutes les mesures composites de risque étudiées, les scores de risque de Framingham montraient la plus forteassociation avec le déclin cognitif. Un risque cardiovasculaire plus élevé était associé à un déclin plus rapide dans de multiples tests cognitifs dont la fluence verbale, le vocabulaire et la cognition globale. Ces résultats suggèrent d’une part qu’un risque cardiovasculaire plus élevé contribue au déclin cognitif dès la phase précoce de vieillissement et d’autre part que l’estimation du risque cardiovasculaire et son effet sur la fonction cognitive nécessite une approche multifactorielle.L’identification et la réduction de facteurs de risque cardiovasculaire peuvent avoir un impact important sur la réduction du déclin cognitif et de la démence. / Several cardiovascular disease risk factors including, dyslipidemia, high blood pressure, and diabetes have been proposed as important modifiable risk factors for cognitive decline and dementia. These risk factors often co-occur and their aggregation is associated with increased risk of cardiovascular disease and dementia. However, studies of composite measures of cardiovascular disease risk in relation to cognitive outcomes in non-elderly populations are scarce. The aim of this thesis was to examine composite measures of risk in relation to cognition and longitudinal cognitive change amongmiddle-aged adults. Data from the Whitehall II study were used to study the associations between the metabolic syndrome, two Framingham risk scores; the Framingham stroke and general cardiovascular disease risk scores, and cognition, based on three cognitive assessments over 10 years. In addition, these two (cardio)vascular risk scores were compared with the CAIDE dementia risk score. Of all composite measures of risk examined, the two Framingham risk scores were the best predictors of 10-year cognitive decline. Higher cardiovascular risk was associated with faster 10-year decline inmultiple cognitive tests including verbal fluency, vocabulary and global cognition. These results suggest that multiple cardiovascular disease risk factors contribute to cognitive decline starting in midlife and that multi-risk factor models such as cardiovascular risk scores may be better suited to assessing risk of cognitive decline. Early identification and treatment of cardiovascular disease risk factors may offer the possibility of markedly delaying or preventing cognitive decline.

Coronary heart disease (CHD) claims millions of lives every year worldwide. In the developed countries, a clear connection has been documented between a decline in CHD mortality and modifiable risk factor reductions. While raising awareness of CHD risk factors reduction is imperative, no valid instrument backed by robust psychometric data is available to measure people‘s awareness in this regard. In addition, especially among the Chinese population, despite many studies already conducted concerning awareness of CHD-related issues, inconsistency in how people define and measure this concept remains. This study aimed to develop a valid instrument that measures Hong Kong Chinese people‘s awareness of CHD risk factors reduction. The study involved two phases. Phase I involved qualitative data collection through 18 focus group interviews (n=100). Participants in this phase included members from three groups: (1) the low risk general public, (2) people having multiple CHD risk factors either with or without CHD, and (3) people who have been diagnosed of myocardial infarction. The objective of this phase was to identify key elements and to clarify the concept inherent in awareness, from which served as a basis to generate items to form the awareness instrument. Upon completion of this phase, three main categories were generated including: CHD knowledge, perceptions of CHD, and risk control efficacy. Under these main categories, twelve subcategories emerged. Under the category of CHD knowledge, the subcategories were: pathological causes of CHD, external forces in causing CHD, modifiable and non-modifiable risk factors, CHD trends, symptoms of CHD, and knowledge of CHD prevention. Under the category of perceptions of CHD, the subcategories were: perceived seriousness of CHD and perceived risk. Under the category of risk control efficacy, the subcategories were: planning of health actions, control over risk reducing behaviour, perceived opportunities to understand CHD, and chest pain appraisal/perceptions. A total of 70 items were generated to form the Awareness of Coronary heart disease Risk Factors Reduction (ACRFR) scale. The second phase of this study focused on the evaluation of the psychometric properties of ACRFR scale. The objective of this phase was to establish the validity and reliability of the instrument. It commenced with determining the content validity by expert review, followed by identifying the factor structure, construct validity and reliability. A good content validity index (CVI) of 0.84 was achieved. The factor structure of ACRFR was identified through exploratory factor analysis (EFA) data collected from a sample (n=232) of the three groups as described in phase one. The final results revealed a seven-factor model with 43 items accounting 49.5% of the total explained variance. The seven factors were: (1) CHD knowledge, (2) planning of health actions, (3) perceived ability to monitor health-related behaviour, (4) perception of risk, (5) perceived opportunities to understand CHD, (6) perceived seriousness of CHD, and (7) chest pain appraisal/perceptions. The factor structure of ACRFR was further cross-validated by confirmatory factor analysis (CFA) in another independent sample (n=225) of the three groups. Goodness of fit statistics fell within acceptable ranges: 2 / d = 1.6, RMSEA = 0.053, NNFI = 0.92, IFI = 0.93, CFI = 0.93. The factor model was further supported by hypothesis testing and known-groups comparisons. The results of hypothesis testing demonstrated significant correlations between ACRFR and other measures. Known-groups comparisons among subjects with MI, those with CHD and without CHD provided satisfactory evidence for construct validity. Reliability of this developed instrument, as estimated by the internal consistency Cronbach‘s alphas, ranged from 0.60 to 0.90 for each sub-scale and for the total scale was 0.82, and the test-retest reliability was 0.89, suggesting good instrument reliability. While current literature reveals no objectively devised conceptual definition of ACRFR and that no published instrument was made available for healthcare professions to enhance people‘s awareness of reducing CHD, this study fills these gaps. It is envisaged that this developed instrument could assist healthcare professional in accurately estimating people‘s awareness of risk factors reduction that could provide valid and reliable data that could inform future directions in CHD prevention and cardiac health promotion.

Doctor of Philosophy (PhD) / Introduction: The conventional approach to weight loss, recommended by almost all health authorities around the world, has been to reduce the total amount of fat in the diet and replace with carbohydrates. However, research trials using this approach have produced only modest results at best, and despite the active promotion of low fat eating and an apparent decline in fat consumption, rates of overweight and obesity have continued to climb. More recently low glycaemic index (GI) and high protein diets have become popular and are widely used by the public. However, only a small number of randomised controlled trials have been conducted and none directly comparing the two. Both approaches effectively reduce glycaemic load (GL) and aim to reduce post-prandial glycaemia and insulinaemia. This study aimed to evaluate the ability of diets with reduced GL to enhance the weight loss effects of a reduced-fat diet, to compare the two approaches of reducing GL on metabolic and anthropometric changes, and to investigate any benefit of combining both approaches to produce the lowest GL. Methods: We conducted a 12-week intervention in 129 overweight or obese young adults who were assigned to one of four diets with varying GL, protein, carbohydrate and GI, but similar fat (30% energy), fat type and fibre content. DIET 1 (highest GL) contained 55% E as carbohydrate; DIET 2 was a low-GI version of DIET 1; DIET 3 was a high protein diet with 25% E as protein; DIET 4 (lowest GL) was a low-GI version of DIET 3. The increase in protein in DIETS 3 and 4 came primarily from lean red meat. All key foods and some pre-prepared frozen meals were provided to maximise dietary compliance. Outcome measures were body weight, body fat, lean mass, waist circumference and the following blood parameters: total cholesterol, LDL-cholesterol, HDL-cholesterol, triacylglycerols (TAG), free fatty acids, C-reactive protein, fasting insulin, fasting glucose and leptin. Insulin resistance and β-cell function were assessed using homeostatic model assessment (HOMA) and the newer computer models HOMA2-insulin sensitivity and HOMA2-β-cell function. Results: While all groups lost similar amounts of weight (4.2 to 6.2% of initial weight, p=0.09), the proportion who lost >5% of body weight varied significantly by diet: 31%, 56%, 66% and 33% in groups 1, 2, 3 and 4 respectively (p=0.011). Differences were strongest in women (76% of the total group) who showed significant differences among groups in percentage weight change (-3.7 ± 0.6%, -5.7 ± 0.6%, -6.5 ± 0.5%, -4.1 ± 0.7% respectively, p=0.005) and fat loss (-3.1 ± 0.4kg, -4.9 ± 0.6kg, -4.8 ± 0.4kg, -3.6 ± 0.7kg respectively, p=0.007). Total and LDL-cholesterol increased on DIET 3 (high protein) compared to a fall on diet 2 (high carbohydrate/low-GI, p=0.013). TAG, HDL-cholesterol and glucose homeostasis improved on all four diets, with no effect of diet composition. Goals for energy distribution were not achieved exactly: both carbohydrate groups ate less fat and the diet 2 group ate more fibre. Conclusions: Reducing GL, through either substituting low-GI foods or replacing some carbohydrate with protein, improved the efficacy of a reduced-fat diet in women and in those with high TAG. Combining both approaches to produce the lowest GL did not promote further weight or body fat loss. Although weight loss was similar in all four diets for the group as a whole, overall clinical outcomes were superior on the high carbohydrate, low-GI diet.

Source: Masters Abstracts International, Volume: 47-06, page: 3373. Advisers: Kelly Volcik; Sarah Baraniuk. Includes bibliographical references.