Inflammation contributes to the etiology of type 2 diabetes (T2D) and cardiovascular disease (CVD). Therefore, it is of interest to investigate how diet relates to plasma inflammatory proteins, particularly whole grain and fibre intakes, as these factors have been associated with lower CVD and T2D risk. Only a limited number of observational studies have examined these relationships. The objective of this study was to investigate the cross-sectional relationships of whole and refined grain and dietary fibre intakes with plasma inflammatory proteins. There was a strong inverse relationship between whole grain intake and plasminogen activator inhibitor type 1 (PAI-1) (β =-0.102; SE=0.038; p=0.0077), and a positive relationship between refined grain intake and PAI-1 (β=0.076; SE=0.034; p=0.0251). Additionally, dietary fibre was related to lower concentrations of C-reactive protein (β=-0.034; SE=0.010; p=0.0008) and fibrinogen (β=-1.207; SE=0.505; p=0.0171). This research suggests that whole and refined grain and fibre intakes may influence inflammatory protein concentrations.

Inflammation contributes to the etiology of type 2 diabetes (T2D) and cardiovascular disease (CVD). Therefore, it is of interest to investigate how diet relates to plasma inflammatory proteins, particularly whole grain and fibre intakes, as these factors have been associated with lower CVD and T2D risk. Only a limited number of observational studies have examined these relationships. The objective of this study was to investigate the cross-sectional relationships of whole and refined grain and dietary fibre intakes with plasma inflammatory proteins. There was a strong inverse relationship between whole grain intake and plasminogen activator inhibitor type 1 (PAI-1) (β =-0.102; SE=0.038; p=0.0077), and a positive relationship between refined grain intake and PAI-1 (β=0.076; SE=0.034; p=0.0251). Additionally, dietary fibre was related to lower concentrations of C-reactive protein (β=-0.034; SE=0.010; p=0.0008) and fibrinogen (β=-1.207; SE=0.505; p=0.0171). This research suggests that whole and refined grain and fibre intakes may influence inflammatory protein concentrations.

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.

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.

The purpose of this dissertation was to examine factors associated with cardiovascular disease (CVD) risk among emerging adults in college aged 18-25 years. CVD risks that develop during this period often persist into adulthood making it an ideal time to target CVD prevention. The specific aims of this dissertation were to 1) explore perceptions of cardiovascular risk among emerging adult men in college; 2) compare differences in unhealthy behaviors and obesity between emerging adults in college living in rural, Appalachian Kentucky and urban Fayette County, Kentucky; and 3) compare measures of general and abdominal obesity in predicting blood pressure among emerging adults in college. Specific Aim One was addressed by a qualitative study of perceptions of cardiovascular risk in 10 emerging adult males in college. Specific Aims Two and Three were addressed by a study of emerging adult college students living in rural, Appalachian and urban Fayette County, Kentucky. We hypothesized that students in rural, Appalachian Kentucky would engage in more unhealthy behaviors and be obese due to living in an austere environment with barriers to healthy behaviors. Although obesity and hypertension are known to be related, researchers have not determined whether body fat distribution, general vs. abdominal, is predictive of blood pressure in emerging adults. Knowing which body fat distribution is the strongest predictor of blood pressure may help in evaluating cardiovascular risk in emerging adults. Emerging adult men emphasized difficulty engaging in CVD health behaviors while attending college and choose to ignore long-term CVD risk. Overcoming college-specific and developmental barriers to engaging in healthy behaviors is critical to reducing cardiovascular risk in this population. Students living in rural, Appalachian Kentucky had more CVD risk behaviors and more were obese compared to those in urban Fayette County, Kentucky. Reducing CVD risk behaviors and obesity among students in rural Appalachian Kentucky may help decrease the high burden of CVD in this region. Findings suggest that waist circumference was the best predictor of systolic blood pressure among emerging adults in college.

The prevalence of obesity in both the developed and developing world have increased, which leads to diverse health outcomes and is placing a heavy burden on the economy. Abdominal obesity proved to be one of the main features in predicting metabolic and cardiovascular disease (CVD) risk and may be the link that unifies the metabolic syndrome (MS) through pro-inflammatory pathways. While the pathogenesis of the MS and each of its components are complex and not well understood, abdominal obesity remains the mechanism that relates to increased lipolysis causing the liver to increase blood glucose and very low lipoprotein output. This in turns leads to raised blood glucose, triglycerides, low-density lipoprotein cholesterol (LDL-C), blood pressure and inflammatory markers (C-reactive protein, interleukin-6 and tumor necrosis factor-a) and decreased high-density lipoprotein cholesterol (HDL-C). Prevention of the metabolic syndrome and treatment of its main characteristics are now considered of utmost importance in order to combat the increased CVD risk and all-cause mortality. Decreasing sedentary behaviour through regular physical activity is a key element in successful treatment of obesity through an increase in energy expenditure, but the ability to decrease low-grade systemic inflammation may be an even greater outcome. Aims The aims of this study was firstly, to determine by means of a literature review, how obesity could be related to a state of chronic systemic inflammation (increased CRP and IL-6). Secondly to determine whether physical activity could serve as a suitable method to decrease inflammation associated with obesity and related disorders. Thirdly to determine if abdominal obesity is a predictor of the metabolic syndrome and CVD and finally, to determine if measures of obesity can predict risk for the metabolic syndrome and CVD risk. Methods For this review study, a computer-assisted literature search were utilized to identify research published between 1990 and 2005. the following databases were utilized for the search: NEXUS, Science Direct, PubMed and Medline. Keywords related to obesity (abdominal obesity, overweight), metabolic syndrome (insulin resistance syndrome, dysmetabolic syndrome, syndrome X), cardiovascular disease (coronary heart disease, coronary artery disease), cardiovascular risk factors (hypertension, dyslipidemia, diabetes mellitus, physical activity), inflammatory markers (CRP, IL-6, chronic low-grade inflammation) and physical activity (fitness, exercise and training) were included as part of the search, including the references identified by previous reviewers (not identified as part of the computerized literature search). Results and conclusions Several research studies concluded that obesity could be an inflammatory disorder due to low-grade systemic inflammation. Adipose tissue is known to be a sectretory organ producing cytokines, acute phase reactants and other circulating factors. The synthesis of adipose tissue TNF-a could induce the production of IL-6, CRP and other acute phase reactants. CRP is a acute phase reactant, synthesized primarily in hepatocytes and secreted by the liver in response to a variety of inflammatory cytokines of which IL-6 and TNF-a are mainly involved. CRP increases rapidly in response to trauma, inflammation and infection. Thus, enhanced levels of CRP can be used as a marker of inflammation. Several studies of large population cohorts provide evidence for an inverse, independent dose-response relation between plasma CRP concentration and level of physical activity in both men and women. Trends for decreased IL-6, TNF-a and CRP concentrations were linear with increasing amounts of reported exercise in most of the research studies, physical activity proved effective in lowering measures of adiposity (BMI, WHR, WC and percentage body fat) and obesity related inflammatory markers (CRP & IL-6). Thereby indicating a potential anti-inflammatory effect. In the studies reviewed in this article abdominal obesity is identified as a predictor and independent risk factor for CVD in both men and women. High levels of deep abdominal fat have also been correlated with components of the metabolic syndrome, glucose intolerance, hyperinsulinemia, hypertension, diabetes, increases in plasma triglyceride levels and a decrease in HDL-C levels (dyslipidemia) in many of the studies. Prospective epidemiological studies have revealed that abdominal obesity (determined by WC and WHR) conveys an independent prediction of CVD risk and is more relevant compared to general obesity (determined by BMI). Abdominal fat has been linked to metabolic risk factors like high systolic blood pressure, atherogenic dyslipidemia, with increased serum TG and decreased HDL-C, and glucose intolerance. Although magnetic resonance imaging (MRI) and computerized tomography (CT) have been used successfully in many studies to measure adipose compartments of the abdomen (subcutaneous and visceral fat), anthropometrical measures like WHR and WC have been proven to be an effective measure in predicting the metabolic syndrome. WC has also been included in the metabolic syndrome definitions of the WHO, ATP Ill and new IDF. / The prevalence of obesity in both the developed and developing world have increased, which leads to diverse health outcomes and is placing a heavy burden on the economy. Abdominal obesity proved to be one of the main features in predicting metabolic and cardiovascular disease (CVD) risk and may be the link that unifies the metabolic syndrome (MS) through pro-inflammatory pathways. While the pathogenesis of the MS and each of its components are complex and not well understood, abdominal obesity remains the mechanism that relates to increased lipolysis causing the liver to increase blood glucose and very low lipoprotein output. This in turns leads to raised blood glucose, triglycerides, low-density lipoprotein cholesterol (LDL-C), blood pressure and inflammatory markers (C-reactive protein, interleukin-6 and tumor necrosis factor-a) and decreased high-density lipoprotein cholesterol (HDL-C). Prevention of the metabolic syndrome and treatment of its main characteristics are now considered of utmost importance in order to combat the increased CVD risk and all-cause mortality. Decreasing sedentary behaviour through regular physical activity is a key element in successful treatment of obesity through an increase in energy expenditure, but the ability to decrease low-grade systemic inflammation may be an even greater outcome. Aims The aims of this study was firstly, to determine by means of a literature review, how obesity could be related to a state of chronic systemic inflammation (increased CRP and IL-6). Secondly to determine whether physical activity could serve as a suitable method to decrease inflammation associated with obesity and related disorders. Thirdly to determine if abdominal obesity is a predictor of the metabolic syndrome and CVD and finally, to determine if measures of obesity can predict risk for the metabolic syndrome and CVD risk. Methods For this review study, a computer-assisted literature search were utilized to identify research published between 1990 and 2005. the following databases were utilized for the search: NEXUS, Science Direct, PubMed and Medline. Keywords related to obesity (abdominal obesity, overweight), metabolic syndrome (insulin resistance syndrome, dysmetabolic syndrome, syndrome X), cardiovascular disease (coronary heart disease, coronary artery disease), cardiovascular risk factors (hypertension, dyslipidemia, diabetes mellitus, physical activity), inflammatory markers (CRP, IL-6, chronic low-grade inflammation) and physical activity (fitness, exercise and training) were included as part of the search, including the references identified by previous reviewers (not identified as part of the computerized literature search). Results and conclusions Several research studies concluded that obesity could be an inflammatory disorder due to low-grade systemic inflammation. Adipose tissue is known to be a sectretory organ producing cytokines, acute phase reactants and other circulating factors. The synthesis of adipose tissue TNF-a could induce the production of IL-6, CRP and other acute phase reactants. CRP is a acute phase reactant, synthesized primarily in hepatocytes and secreted by the liver in response to a variety of inflammatory cytokines of which IL-6 and TNF-a are mainly involved. CRP increases rapidly in response to trauma, inflammation and infection. Thus, enhanced levels of CRP can be used as a marker of inflammation. Several studies of large population cohorts provide evidence for an inverse, independent dose-response relation between plasma CRP concentration and level of physical activity in both men and women. Trends for decreased IL-6, TNF-a and CRP concentrations were linear with increasing amounts of reported exercise in most of the research studies, physical activity proved effective in lowering measures of adiposity (BMI, WHR, WC and percentage body fat) and obesity related inflammatory markers (CRP & IL-6). Thereby indicating a potential anti-inflammatory effect. In the studies reviewed in this article abdominal obesity is identified as a predictor and independent risk factor for CVD in both men and women. High levels of deep abdominal fat have also been correlated with components of the metabolic syndrome, glucose intolerance, hyperinsulinemia, hypertension, diabetes, increases in plasma triglyceride levels and a decrease in HDL-C levels (dyslipidemia) in many of the studies. Prospective epidemiological studies have revealed that abdominal obesity (determined by WC and WHR) conveys an independent prediction of CVD risk and is more relevant compared to general obesity (determined by BMI). Abdominal fat has been linked to metabolic risk factors like high systolic blood pressure, atherogenic dyslipidemia, with increased serum TG and decreased HDL-C, and glucose intolerance. Although magnetic resonance imaging (MRI) and computerized tomography (CT) have been used successfully in many studies to measure adipose compartments of the abdomen (subcutaneous and visceral fat), anthropometrical measures like WHR and WC have been proven to be an effective measure in predicting the metabolic syndrome. WC has also been included in the metabolic syndrome definitions of the WHO, ATP Ill and new IDF. / Thesis (M.A. (Human Movement Science))--North-West University, Potchefstroom Campus, 2006.

The prevalence of obesity in both the developed and developing world have increased, which leads to diverse health outcomes and is placing a heavy burden on the economy. Abdominal obesity proved to be one of the main features in predicting metabolic and cardiovascular disease (CVD) risk and may be the link that unifies the metabolic syndrome (MS) through pro-inflammatory pathways. While the pathogenesis of the MS and each of its components are complex and not well understood, abdominal obesity remains the mechanism that relates to increased lipolysis causing the liver to increase blood glucose and very low lipoprotein output. This in turns leads to raised blood glucose, triglycerides, low-density lipoprotein cholesterol (LDL-C), blood pressure and inflammatory markers (C-reactive protein, interleukin-6 and tumor necrosis factor-a) and decreased high-density lipoprotein cholesterol (HDL-C). Prevention of the metabolic syndrome and treatment of its main characteristics are now considered of utmost importance in order to combat the increased CVD risk and all-cause mortality. Decreasing sedentary behaviour through regular physical activity is a key element in successful treatment of obesity through an increase in energy expenditure, but the ability to decrease low-grade systemic inflammation may be an even greater outcome. Aims The aims of this study was firstly, to determine by means of a literature review, how obesity could be related to a state of chronic systemic inflammation (increased CRP and IL-6). Secondly to determine whether physical activity could serve as a suitable method to decrease inflammation associated with obesity and related disorders. Thirdly to determine if abdominal obesity is a predictor of the metabolic syndrome and CVD and finally, to determine if measures of obesity can predict risk for the metabolic syndrome and CVD risk. Methods For this review study, a computer-assisted literature search were utilized to identify research published between 1990 and 2005. the following databases were utilized for the search: NEXUS, Science Direct, PubMed and Medline. Keywords related to obesity (abdominal obesity, overweight), metabolic syndrome (insulin resistance syndrome, dysmetabolic syndrome, syndrome X), cardiovascular disease (coronary heart disease, coronary artery disease), cardiovascular risk factors (hypertension, dyslipidemia, diabetes mellitus, physical activity), inflammatory markers (CRP, IL-6, chronic low-grade inflammation) and physical activity (fitness, exercise and training) were included as part of the search, including the references identified by previous reviewers (not identified as part of the computerized literature search). Results and conclusions Several research studies concluded that obesity could be an inflammatory disorder due to low-grade systemic inflammation. Adipose tissue is known to be a sectretory organ producing cytokines, acute phase reactants and other circulating factors. The synthesis of adipose tissue TNF-a could induce the production of IL-6, CRP and other acute phase reactants. CRP is a acute phase reactant, synthesized primarily in hepatocytes and secreted by the liver in response to a variety of inflammatory cytokines of which IL-6 and TNF-a are mainly involved. CRP increases rapidly in response to trauma, inflammation and infection. Thus, enhanced levels of CRP can be used as a marker of inflammation. Several studies of large population cohorts provide evidence for an inverse, independent dose-response relation between plasma CRP concentration and level of physical activity in both men and women. Trends for decreased IL-6, TNF-a and CRP concentrations were linear with increasing amounts of reported exercise in most of the research studies, physical activity proved effective in lowering measures of adiposity (BMI, WHR, WC and percentage body fat) and obesity related inflammatory markers (CRP & IL-6). Thereby indicating a potential anti-inflammatory effect. In the studies reviewed in this article abdominal obesity is identified as a predictor and independent risk factor for CVD in both men and women. High levels of deep abdominal fat have also been correlated with components of the metabolic syndrome, glucose intolerance, hyperinsulinemia, hypertension, diabetes, increases in plasma triglyceride levels and a decrease in HDL-C levels (dyslipidemia) in many of the studies. Prospective epidemiological studies have revealed that abdominal obesity (determined by WC and WHR) conveys an independent prediction of CVD risk and is more relevant compared to general obesity (determined by BMI). Abdominal fat has been linked to metabolic risk factors like high systolic blood pressure, atherogenic dyslipidemia, with increased serum TG and decreased HDL-C, and glucose intolerance. Although magnetic resonance imaging (MRI) and computerized tomography (CT) have been used successfully in many studies to measure adipose compartments of the abdomen (subcutaneous and visceral fat), anthropometrical measures like WHR and WC have been proven to be an effective measure in predicting the metabolic syndrome. WC has also been included in the metabolic syndrome definitions of the WHO, ATP Ill and new IDF. / The prevalence of obesity in both the developed and developing world have increased, which leads to diverse health outcomes and is placing a heavy burden on the economy. Abdominal obesity proved to be one of the main features in predicting metabolic and cardiovascular disease (CVD) risk and may be the link that unifies the metabolic syndrome (MS) through pro-inflammatory pathways. While the pathogenesis of the MS and each of its components are complex and not well understood, abdominal obesity remains the mechanism that relates to increased lipolysis causing the liver to increase blood glucose and very low lipoprotein output. This in turns leads to raised blood glucose, triglycerides, low-density lipoprotein cholesterol (LDL-C), blood pressure and inflammatory markers (C-reactive protein, interleukin-6 and tumor necrosis factor-a) and decreased high-density lipoprotein cholesterol (HDL-C). Prevention of the metabolic syndrome and treatment of its main characteristics are now considered of utmost importance in order to combat the increased CVD risk and all-cause mortality. Decreasing sedentary behaviour through regular physical activity is a key element in successful treatment of obesity through an increase in energy expenditure, but the ability to decrease low-grade systemic inflammation may be an even greater outcome. Aims The aims of this study was firstly, to determine by means of a literature review, how obesity could be related to a state of chronic systemic inflammation (increased CRP and IL-6). Secondly to determine whether physical activity could serve as a suitable method to decrease inflammation associated with obesity and related disorders. Thirdly to determine if abdominal obesity is a predictor of the metabolic syndrome and CVD and finally, to determine if measures of obesity can predict risk for the metabolic syndrome and CVD risk. Methods For this review study, a computer-assisted literature search were utilized to identify research published between 1990 and 2005. the following databases were utilized for the search: NEXUS, Science Direct, PubMed and Medline. Keywords related to obesity (abdominal obesity, overweight), metabolic syndrome (insulin resistance syndrome, dysmetabolic syndrome, syndrome X), cardiovascular disease (coronary heart disease, coronary artery disease), cardiovascular risk factors (hypertension, dyslipidemia, diabetes mellitus, physical activity), inflammatory markers (CRP, IL-6, chronic low-grade inflammation) and physical activity (fitness, exercise and training) were included as part of the search, including the references identified by previous reviewers (not identified as part of the computerized literature search). Results and conclusions Several research studies concluded that obesity could be an inflammatory disorder due to low-grade systemic inflammation. Adipose tissue is known to be a sectretory organ producing cytokines, acute phase reactants and other circulating factors. The synthesis of adipose tissue TNF-a could induce the production of IL-6, CRP and other acute phase reactants. CRP is a acute phase reactant, synthesized primarily in hepatocytes and secreted by the liver in response to a variety of inflammatory cytokines of which IL-6 and TNF-a are mainly involved. CRP increases rapidly in response to trauma, inflammation and infection. Thus, enhanced levels of CRP can be used as a marker of inflammation. Several studies of large population cohorts provide evidence for an inverse, independent dose-response relation between plasma CRP concentration and level of physical activity in both men and women. Trends for decreased IL-6, TNF-a and CRP concentrations were linear with increasing amounts of reported exercise in most of the research studies, physical activity proved effective in lowering measures of adiposity (BMI, WHR, WC and percentage body fat) and obesity related inflammatory markers (CRP & IL-6). Thereby indicating a potential anti-inflammatory effect. In the studies reviewed in this article abdominal obesity is identified as a predictor and independent risk factor for CVD in both men and women. High levels of deep abdominal fat have also been correlated with components of the metabolic syndrome, glucose intolerance, hyperinsulinemia, hypertension, diabetes, increases in plasma triglyceride levels and a decrease in HDL-C levels (dyslipidemia) in many of the studies. Prospective epidemiological studies have revealed that abdominal obesity (determined by WC and WHR) conveys an independent prediction of CVD risk and is more relevant compared to general obesity (determined by BMI). Abdominal fat has been linked to metabolic risk factors like high systolic blood pressure, atherogenic dyslipidemia, with increased serum TG and decreased HDL-C, and glucose intolerance. Although magnetic resonance imaging (MRI) and computerized tomography (CT) have been used successfully in many studies to measure adipose compartments of the abdomen (subcutaneous and visceral fat), anthropometrical measures like WHR and WC have been proven to be an effective measure in predicting the metabolic syndrome. WC has also been included in the metabolic syndrome definitions of the WHO, ATP Ill and new IDF. / Thesis (M.A. (Human Movement Science))--North-West University, Potchefstroom Campus, 2006.

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.

京都大学 / 新制・課程博士 / 博士(工学) / 甲第23494号 / 工博第4906号 / 新制||工||1766(附属図書館) / 京都大学大学院工学研究科都市環境工学専攻 / (主査)教授 高野 裕久, 教授 米田 稔, 准教授 上田 佳代 / 学位規則第4条第1項該当 / Doctor of Philosophy (Engineering) / Kyoto University / DFAM

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.