Type 1 diabetes (T1D) is characterised by an absolute insulin deficiency resulting from the chronic and progressive destruction of pancreatic β-cells by the immune system cells. Continuous subcutaneous insulin infusion (CSII) is becoming a popular technique for insulin delivery among T1D patients. Exercise is known to exert anti-inflammatory effects and metabolic control. Therefore it was of interest to study this in T1D using CSII. The objectives of this thesis were to further understanding of the effect of exercise on blood glucose, hemoglobin A1c, lipids, insulin and inflammatory markers in healthy and T1D volunteers. Three studies have been investigated where the diabetic volunteers used multi daily injections (MDI) or CSII. Firstly a survey was conducted aimed to investigate the effect of exercise on T1D patients using CSII therapy. The second study examined the acute and chronic effects of resistance and cardio exercise at moderate intensity on inflammatory markers such as IL-6, IL-1β, TNF-α and IFN-γ in healthy and T1D using MDI or CSII. Finally, a study was undertaken to find out the effects of chronic moderate intensity exercise on lipids profile and glycaemic control in healthy and T1D using MDI or CSII. The statistical analysis of the survey showed that CSII therapy for T1D had a significant reduction on A1c, insulin requirement and improvement of lipids profile compared to MDI. Moreover, majority of CSII users (63%) rarely suffered from hypoglycemia during exercise. The second study demonstrated that acute and chronic exercises have a positive impact on the inflammatory markers among CSII users e.g. in CSII users statistically significant increase in IL-6 and TNF-α levels were observed (P=0.014 and P=0.001 respectively). The last study showed that lipids profile, total daily insulin units were improved and A1c levels were significantly reduced in CSII as well as MDI groups after 6 weeks of exercise. T1D affects major organs e.g. heart, kidneys, blood vessels etc. However, good glycaemic control can reduce the risk of diabetes complications. This study suggested that CSII therapy along with exercise can maintain the BG level close to normal, as all 5 participants of the study showed an improvement in their BG levels after exercise.

Objetivo: Este trabalho avaliou as condições periodontais em mulheres com câncer de mama, sob tratamento quimioterápico, e monitorou o efeito do tratamento periodontal nas condições clínicas e sistêmicas dessas pacientes. Materiais e Métodos As pacientes foram divididas em quatro grupos: pacientes controles saudáveis (SAU) (n=16); pacientes com câncer e sem doença periodontal (CAN) (n=15); pacientes que não tinham câncer porém que tinham doença periodontal (DP) (n=18); e pacientes com câncer e com doença periodontal (CAN-DP) (n=10). Os parâmetros clínicos avaliados foram: Índice de Placa (IP), Índice Gengival (IG), Profundidade de Sondagem (PS), Nível Clínico de Inserção (NCI) e os parâmetros hematológicos (proteína C-reativa-PCR) e a contagem total de neutrófilos (PMN) foram avaliados no baseline, aos 45 dias e aos 90 dias após terapia periodontal não-cirúrgica. Resultados: No baseline, os grupos DP e CAN-DP exibiram maiores valores de PS, NCI, IP, IG (p&#9633; 0,01 e p&#9633;0,01) do que os grupos SAU e CAN. Os níveis de PCR não apresentaram diferença estatística (p>0,05) entre os grupos experimentais, e a contagem de neutrófilos foi estatisticamente maior para o grupo DP (p<0,05). Após o tratamento periodontal, observou-se uma redução significativa (p<0,05) de PS no grupo CAN e no grupo DP aos 90 dias em relação ao baseline. O grupo DP exibiu um ganho de inserção clínica significante aos 45 e 90 dias em relação ao baseline (p<0,05). Houve redução significativa do índice de placa aos 45 e 90 dias para os grupos SAU, DP e CAN-DP (p&#9633;0,05). Todos os grupos exibiram redução significativa no IG tanto ao 45 quanto aos 90 dias (p<0,05). Entretanto, aos 90 dias, essa redução foi estatisticamente maior para o grupo SAU do que para o grupo CAN (p<0,05). Aos 90 dias pós-tratamento periodontal, o grupo CAN-DP exibiu maior frequência de bolsas residuais (p<0,05), menor redução de profundidade de sondagem (p<0,05) e maior risco de progressão da doença (p<0,05) do que o grupo DP. Os grupos PD e CAN apresentaram uma redução nos níveis da PCR aos 45 dias. Esta redução foi estatisticamente significativa para o grupo PC e CAN, além disso, o grupo CAN mostrou uma diferença estatisticamente significativa aos 90 dias quando comparado ao baseline. O grupo DP teve uma significativa redução de neutrófilos aos 45 dias, quando comparado aos valores do baseline. Conclusão: Os resultados deste estudo não conseguiram detectar a associação entre doença periodontal e câncer. Embora o tratamento periodontal reduz os marcadores clínicos inflamatórios de gengivite e de periodontite e os parâmetros hematológicos tanto em pacientes saudáveis como nos pacientes com câncer e em quimioterapia. Porém, essa redução é mais palpável nos pacientes sem câncer mostrando que a doença e/ou a quimioterapia prejudica o controle inflamatório. / The association between periodontal disease and cancer has been recently established and the logic behind it is that inflammation is a common factor between both diseases, although all the involved mechanisms in this association have to be clarified. Furthermore, periodontal infection/inflammation may be aggravated during chemotherapy and contribute for systemic inflammatory process. Objective: This study compared the periodontal status in healthy and breast cancer patients before chemotherapy and monitored the effect of periodontal treatment in the clinical and systemic conditions. Materials and Methods: The subjects were allocated into four groups: healthy patients (H) (n = 16); cancer patients without periodontal disease (CAN) (n = 15); periodontally compromised patients (PC) (n = 18); and cancer and periodontally compromised patients (CAN-PC) (n = 10). The clinical parameters: probing depth (PD), clinical attachment level (CAL), plaque index (PI) and gingival index (GI); the hematological parameters: C-reactive-protein (CRP) and neutrophils (PMN) were accessed at baseline, 45 and 90 days after non-surgical periodontal therapy. The differences intra and inter-groups were verified by the analysis of variance of two criteria followed by the Post-Hoc test of Bonferroni (p<0,05) and for hematologic parameters were verified by the Friedman test and by the Mann-Whitney test (p<0,05). Results: At baseline, there was no difference between the two periodontally healthy and the two periodontally compromised groups regarding the clinical parameters; there were no statistically significant differences for PCR; and PMN were statistically higher for the PC groups (p&#9633;0,05). After the periodontal treatment there was a significant reduction (p&#9633;0,05) of PD in the CAN group and in the PC group at 90 days post therapy comparing to baseline (p&#9633;0,05). There was a significant reduction on the PI at 45 and 90 days for the H group, PC and CAN-PC groups (p&#9633;0,05). All groups had a significant reduction on GI at 45 and 90 days after treatment (p&#9633;0,05). However, this reduction was statistically more pronounced in the H group than in the CAN group (p&#9633;0,05). At 90 days post periodontal treatment, the CAN-PC group exhibited a greater frequency of residual periodontal pockets (p&#9633;0,05), less PD reduction (p&#9633;0,05) and a greater risk of periodontitis progression (p&#9633;0,05) than the PC patients. The PC and the CAN groups showed a statically significant reduction in PCR levels at 45 days (p<0,05), furthermore the CAN group showed also statistically significant differences reduction in PCR levels at 90 days (p<0,05). The PC group had a significant reduction in the PMN at 45 days when compared to baseline values. Conclusion: The results of this study have failed to detect the association between periodontal disease and cancer. The periodontal treatment reduces the inflammatory markers of gingivitis and periodontitis and the hematological markers, however, this reduction is more pronounced in patients without cancer, showing that the disease and/or the chemotherapy impair the inflammatory control.

Objetivo: Este trabalho avaliou as condições periodontais em mulheres com câncer de mama, sob tratamento quimioterápico, e monitorou o efeito do tratamento periodontal nas condições clínicas e sistêmicas dessas pacientes. Materiais e Métodos As pacientes foram divididas em quatro grupos: pacientes controles saudáveis (SAU) (n=16); pacientes com câncer e sem doença periodontal (CAN) (n=15); pacientes que não tinham câncer porém que tinham doença periodontal (DP) (n=18); e pacientes com câncer e com doença periodontal (CAN-DP) (n=10). Os parâmetros clínicos avaliados foram: Índice de Placa (IP), Índice Gengival (IG), Profundidade de Sondagem (PS), Nível Clínico de Inserção (NCI) e os parâmetros hematológicos (proteína C-reativa-PCR) e a contagem total de neutrófilos (PMN) foram avaliados no baseline, aos 45 dias e aos 90 dias após terapia periodontal não-cirúrgica. Resultados: No baseline, os grupos DP e CAN-DP exibiram maiores valores de PS, NCI, IP, IG (p&#9633; 0,01 e p&#9633;0,01) do que os grupos SAU e CAN. Os níveis de PCR não apresentaram diferença estatística (p>0,05) entre os grupos experimentais, e a contagem de neutrófilos foi estatisticamente maior para o grupo DP (p<0,05). Após o tratamento periodontal, observou-se uma redução significativa (p<0,05) de PS no grupo CAN e no grupo DP aos 90 dias em relação ao baseline. O grupo DP exibiu um ganho de inserção clínica significante aos 45 e 90 dias em relação ao baseline (p<0,05). Houve redução significativa do índice de placa aos 45 e 90 dias para os grupos SAU, DP e CAN-DP (p&#9633;0,05). Todos os grupos exibiram redução significativa no IG tanto ao 45 quanto aos 90 dias (p<0,05). Entretanto, aos 90 dias, essa redução foi estatisticamente maior para o grupo SAU do que para o grupo CAN (p<0,05). Aos 90 dias pós-tratamento periodontal, o grupo CAN-DP exibiu maior frequência de bolsas residuais (p<0,05), menor redução de profundidade de sondagem (p<0,05) e maior risco de progressão da doença (p<0,05) do que o grupo DP. Os grupos PD e CAN apresentaram uma redução nos níveis da PCR aos 45 dias. Esta redução foi estatisticamente significativa para o grupo PC e CAN, além disso, o grupo CAN mostrou uma diferença estatisticamente significativa aos 90 dias quando comparado ao baseline. O grupo DP teve uma significativa redução de neutrófilos aos 45 dias, quando comparado aos valores do baseline. Conclusão: Os resultados deste estudo não conseguiram detectar a associação entre doença periodontal e câncer. Embora o tratamento periodontal reduz os marcadores clínicos inflamatórios de gengivite e de periodontite e os parâmetros hematológicos tanto em pacientes saudáveis como nos pacientes com câncer e em quimioterapia. Porém, essa redução é mais palpável nos pacientes sem câncer mostrando que a doença e/ou a quimioterapia prejudica o controle inflamatório. / The association between periodontal disease and cancer has been recently established and the logic behind it is that inflammation is a common factor between both diseases, although all the involved mechanisms in this association have to be clarified. Furthermore, periodontal infection/inflammation may be aggravated during chemotherapy and contribute for systemic inflammatory process. Objective: This study compared the periodontal status in healthy and breast cancer patients before chemotherapy and monitored the effect of periodontal treatment in the clinical and systemic conditions. Materials and Methods: The subjects were allocated into four groups: healthy patients (H) (n = 16); cancer patients without periodontal disease (CAN) (n = 15); periodontally compromised patients (PC) (n = 18); and cancer and periodontally compromised patients (CAN-PC) (n = 10). The clinical parameters: probing depth (PD), clinical attachment level (CAL), plaque index (PI) and gingival index (GI); the hematological parameters: C-reactive-protein (CRP) and neutrophils (PMN) were accessed at baseline, 45 and 90 days after non-surgical periodontal therapy. The differences intra and inter-groups were verified by the analysis of variance of two criteria followed by the Post-Hoc test of Bonferroni (p<0,05) and for hematologic parameters were verified by the Friedman test and by the Mann-Whitney test (p<0,05). Results: At baseline, there was no difference between the two periodontally healthy and the two periodontally compromised groups regarding the clinical parameters; there were no statistically significant differences for PCR; and PMN were statistically higher for the PC groups (p&#9633;0,05). After the periodontal treatment there was a significant reduction (p&#9633;0,05) of PD in the CAN group and in the PC group at 90 days post therapy comparing to baseline (p&#9633;0,05). There was a significant reduction on the PI at 45 and 90 days for the H group, PC and CAN-PC groups (p&#9633;0,05). All groups had a significant reduction on GI at 45 and 90 days after treatment (p&#9633;0,05). However, this reduction was statistically more pronounced in the H group than in the CAN group (p&#9633;0,05). At 90 days post periodontal treatment, the CAN-PC group exhibited a greater frequency of residual periodontal pockets (p&#9633;0,05), less PD reduction (p&#9633;0,05) and a greater risk of periodontitis progression (p&#9633;0,05) than the PC patients. The PC and the CAN groups showed a statically significant reduction in PCR levels at 45 days (p<0,05), furthermore the CAN group showed also statistically significant differences reduction in PCR levels at 90 days (p<0,05). The PC group had a significant reduction in the PMN at 45 days when compared to baseline values. Conclusion: The results of this study have failed to detect the association between periodontal disease and cancer. The periodontal treatment reduces the inflammatory markers of gingivitis and periodontitis and the hematological markers, however, this reduction is more pronounced in patients without cancer, showing that the disease and/or the chemotherapy impair the inflammatory control.

Herpes simplex viruses (HSVs), are among the most virulent and widespread pathogens; they affect 60-90% of the population worldwide. Substantial evidence indicates a possible association between pathogens and chronic disease. HSVs, among other viruses, have been associated with increased risk for inflammatory diseases. However, prior findings have been inconsistent on the role of infection in triggering autoimmune response and chronic disease. This study builds on the premise that pathogens can induce an inflammatory response and increase the risk for disease development. A representative U.S. sample from NHANES, a national population-based cross-sectional survey, was used to examine the relationship between HSVs infection and type 2 diabetes mellitus (T2DM) and cardiovascular disease (CVD). Results from the two-tailed, Pearson chi-square test and multiple logistic regression analyses found no significant association between HSV or multiple herpes virus infections and T2DM or CVD, which suggest rather a secondary phenomenon. However, all the risk factors examined in this study indicated an association with either T2DM, CVD or both. Two inflammatory markers, C-reactive protein (CRP) and serum ferritin, were significantly associated with T2DM and CVD. These findings have potential implications for social change as they support the premise that high levels of CRP and ferritin may be associated with T2DM and CVD. Existing guidelines for primary and secondary prevention of T2DM and CVD could be expanded (a) to include CRP and ferritin as part of the health assessment for T2DM and CVD in high-risk populations, and (b) to explore the effectiveness of CRP and ferritin as predictive biomarkers and prognostic tools for T2DM and CVD.

Polycyclic aromatic hydrocarbons (PAHs) are environmental and occupational carcinogens that are produced by the incomplete combustion of organic material, such as from the burning of tobacco, coal, and petroleum products. In addition to causing cancer, exposure to PAHs is hypothesized to contribute to atherosclerosis and to lead to increased incidence rates of cardiovascular disease in populations. Considering the number of deaths attributable to tobacco smoke exposure, ambient air pollution, and occupational hazards, PAHs may be a significant contributor to the prevalence of cardiovascular disease in human populations. However, a clear exposure-response relationship between PAHs and measures of cardiovascular disease has not been demonstrated. While PAH exposure has been shown to be associated with indicators of cardiovascular disease in research animals, this relationship has not been studied comprehensively in human populations. Using data from the continuous National Health and Nutrition Examination Surveys (NHANES) 1999 - 2004 of a representative sample of the entire US civilian population, this study investigated predictors of total body burden of PAHs and associations between urinary metabolites of PAHs and biomarkers of cardiovascular disease in 4,492 study participants aged 20 years and older. Using various analytic approaches, this research project identified tobacco smoke exposure as a significant predictor of urinary levels of low molecular weight PAHs but not as a predictor of urinary levels of high molecular weight PAHs in a large population of individuals without known occupational exposure to PAHs. Worker occupational category was not associated with urinary levels of any PAH metabolites. The results of this study also indicate a possible association between exposure to PAHs and the development of cardiovascular disease in humans. Levels of multiple metabolites of specific PAHs, naphthalene, fluorene, and phenanthrene were significantly associated with increases in total cholesterol, triglycerides, WBC count, and C-reactive protein levels. Additionally, this study examined the utility of factor analysis for data reduction of 23 urinary PAH metabolites to two latent factors representing low and high molecular weight PAHs to streamline investigations of the associations of PAH exposures with various health outcomes. Results of this study suggest mechanisms by which PAH exposure contributes to the burden of cardiovascular disease on human populations and the methods by which human body burden on PAHs can be measured.

Polycystic ovary syndrome (PCOS) is one of the most common endocrine disorders among women of childbearing age and is associated with a number of metabolic disturbances. It has been hypothesised these women carry an increased risk of developing cardiovascular diseases (CVD) with advancing age. The first aim of this thesis was to establish the prevalence of PCOS-related symptoms in Northern Sweden. The Northern part of the WHO MONICA project was used for this purpose. Based on self-reported menstrual disturbances and hirsutism together with biochemical analyses of free androgen index, the estimated prevalence of PCOS in Northern Sweden was 4.8%, which corresponded with previous prevalence studies. Disturbances in the fibrinolytic system are predictors of future cardiovascular events and measurements of plasminogen activator inhibitor 1 (PAI-1) activity and tissue plasminogen activator (tPA) mass concentration may be used to assess fibrinolytic activity in women with PCOS. From the findings, over-weight women with PCOS had impaired fibrinolysis, especially if they displayed objective biochemical markers of hyperandrogenism. Conversely, lean women with PCOS, displayed no signs of disturbed fibrinolysis. The adipose tissue is an active endocrine organ that produces and releases hormones, pro- and anti-inflammatory cytokines, and chemoattractant cytokines. Proinflammatory molecules produced by adipose tissue can be active participants in the development of insulin resistance and the increased risk of cardiovascular disease associated with obesity. The findings suggested being overweight, rather than the PCOS diagnosis per se, was the main explanatory variable for elevated adipose tissue inflammation in PCOS patients. Weight reduction is the primary target for intervention in overweight and obese women with PCOS. When this thesis was planned, no placebo-controlled trials on anti-obesity drugs in women with PCOS had been conducted. Sibutramine in combination with lifestyle intervention resulted in significant weight reduction in overweight women with PCOS. In addition to the weight loss, sibutramine appeared to have a beneficial effect on metabolic and cardiovascular risk factors.

This study investigated whether or not there was an overall difference in the pulmonary oxidative marker, 8-isoprostane (PGF2-a), found in exhaled breath condensate, during pregnancy versus the non-pregnant state. The utility of this information was important secondary to the effect of maternal asthma on pregnancy and outcome, as it has been demonstrated in past studies that overall pregnant females with asthma have been shown to have an increased risk of exacerbation requiring medical intervention.The primary goal of this study sought to determine if there is a difference in PGF2a levels in the exhaled breath condensate of pregnant versus non-pregnant females. In order to achieve this goal a cross-sectional study was performed consisting of two groups and were compared to one another. A group of 16 healthy, non-pregnant females aged 18-35 years old was compared to a group of 6 healthy, pregnant females in their third trimester of pregnancy. Both groups exhaled breath condensate was collected and 8-isoprostane levels determined and compared to each other. Both groups compared did not report a history of environmental allergies, asthma, and smoking. The non-pregnant group showed a mean 8-isoprostane level of 11.513pg/ml (C.I. 8.7633- 14.263). The pregnant group showed a mean 8-isoprostane level of 17.34 pg/ml (C.I. -4.209-38.889).Although a crude observable difference between the means of the two groups was determined, this pilot study did not show a statistically significant difference between the means of the pregnant versus non-pregnant group when they were statistically compared. This finding is primarily due to the small sample size of both groups. A power calculation determined that each group would require 25 participants in order to establish a statistically significant difference in the 8-isoprostane levels in exhaled breath condensate. The implication is that a larger scale study is needed in order to conclusively determine if there is a statistically significant difference between the exhaled breath condensate 8-isoprostane levels in pregnant versus non-pregnant females.

African Americans experience a disproportionate mortality, morbidity, and disability associated with ischemic stroke. Traditional risk factors offer some explanation for this finding, but novel risk factors have not been explored. APOE4 genotype, which is more prevalent in African Americans demonstrate a pro-inflammatory phenotype that may result in an exaggerated inflammatory response associated with ischemic stroke, resulting in worse outcomes. The purpose of this study was to examine relationships among APOE genotypes, inflammatory markers (CD11β, platelet leukocyte aggregates, IL-1β, IL-6, IL-8, and tissue necrosis factor alpha), the anti-inflammatory marker, IL-10, and risk factors (hypertension, diabetes type II, obesity, hyperlipidemia, and smoking) in African Americans at 3 days post stroke. Twenty five patients were enrolled with 12 patients in the APOE4 group and 13 patients in the non-APOE4 group. In the APOE4 group, 75% were male compared to 54% in the non-APOE4 group. The average age in the APOE4 group was 56.5 ± 9.0 compared to 66 ± 16.0 years in the non-APOE4 group. Females in the APOE4 group were younger with ages comparable to men. All participants had hypertension. Forty two percent of patients in the APOE4 group had two risk factors and 46% of patients in the non-APOE4 group had three risk factors. Major findings included 1) there were no statistical difference between inflammatory markers and APOE genotypes, and 2) the APOE4 carrier was not a predictor for overall inflammatory load among African Americans with ischemic stroke. The study was underpowered and small effect sizes were not sufficient to create statistical findings. This was the first study to examined APOE genotypes, inflammatory markers, and risk factors among African Americans with ischemic stroke. More studies are needed to not only investigate novel risk factors, but to also characterize inflammatory and genetic mechanisms with ischemic stroke and their associated outcomes among African Americans. Such studies may lead to primary and secondary prevention of ischemic stroke and reduce the health disparities associated with ischemic stroke among African Americans.

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.