Orientador: Sílvia Justina Papini / Resumo: Introdução: A esquizofrenia é uma doença crônica e o tratamento acontece com utilização de fármacos antipsicóticos de modo prolongado. As medicações controlam os sintomas da doença, melhoram o bem-estar do indivíduo e elevam a chance de adaptação ao meio social, em contrapartida, acarretam vários efeitos adversos, sendo a alteração dos componentes da síndrome metabólica a mais comum. Objetivo: Avaliar o efeito da suplementação de farelo de aveia sobre o peso corporal, circunferência abdominal e componentes da síndrome metabólica de pacientes psicóticos institucionalizados em um hospital psiquiátrico. Método: Trata-se de um estudo quantitativo com intervenção em indivíduos psicóticos crônicos. A partir da medida de peso e estatura calculou-se o índice de massa corporal (IMC) para classificação do estado nutricional nos 4 momentos do estudo, início, 90 e180 dias de suplementação e 180 dias após o término da suplementação. Foram avaliados os componentes da síndrome metabólica: circunferência abdominal, glicemia de jejum, HDL-colesterol, triglicerídeos, antes e ao final da suplementação e após 180 dias sem suplementação. Resultados: Foram estudados todos os 45 moradores do local, destes, 62% eram do sexo masculino, com a média de idade de 55,5± 13,2 anos, todos há mais de cinco anos internados. Na sua totalidade faziam uso de medicação antipsicótica, 75% deles apresentaram risco cardiovascular, 46,7% eram obesos, 33,3% apresentaram colesterol total elevado, 50% hipertrigliceridem... (Resumo completo, clicar acesso eletrônico abaixo) / Abstract: Introduction: Schizophrenia is a chronic disease and treatment occurs with prolonged use of antipsychotic drugs. The medications control the symptoms of the disease, improve the well-being of the individual and increase the chance of adaptation to the social environment. On the other hand, medications have several adverse effects, and the alteration of the components of the metabolic syndrome is the most common. Objective: To evaluate the effect of supplementation of oat bran on body weight, abdominal circumference and components of the metabolic syndrome of institutionalized psychotic patients in a psychiatric hospital. Method: This is a quantitative study with intervention in chronic psychotic individuals. Body mass index (BMI) was calculated from the body mass index (BMI) for the classification of the nutritional status in the 4 study moments, beginning, 90 and 180 days of supplementation and 180 days after the end of the supplementation. The components of the metabolic syndrome: abdominal circumference, fasting glucose, HDL-cholesterol, triglycerides, before and at the end of the supplementation, and after 180 days without supplementation, were evaluated. Results: All 45 residents were studied. Of these, 62% were male, with a mean age of 55.5 ± 13.2 years, all of whom had been hospitalized for more than five years. 75% of them had a cardiovascular risk, 46.7% were obese, 33.3% had high total cholesterol, 50% had hypertriglyceridemia, 28.9% had arterial hypertension and 88... (Complete abstract click electronic access below) / Mestre

Abstract Metabolic Syndrome (MetSyn) is a medical condition prevalent in Australia. MetSyn is diagnosed with a varying combination of visceral obesity, insulin resistance/ impaired glucose tolerance/ Type 2 diabetes, dyslipidaemia and hypertension. Obesity is a central feature of this syndrome that is characterised by abnormalities in glucose and lipid metabolism. An understanding of the cause of the metabolic derangement that occurs in obesity, and that contributes to MetSyn, would allow effective treatment and prevention strategies to be formulated. This is a priority in the current environment of highly prevalent overweight and obesity in Australian children and adults. Lipotoxicity of insulin-dependent tissues and ectopic fat depots are emerging as fundamental processes in the pathogenesis of MetSyn. Lifestyle intervention, such as increased physical activity, show great promise as agents for disrupting the disease progression and may act via direct or indirect mechanisms on the underlying pathology of MetSyn. This study aimed to determine if diagnostic markers of MetSyn exist in obese, prepubertal, Australian children and to assess the contribution of lifestyle factors on components of MetSyn. Further, this study sought to investigate the relationship between body fat patterning (total body fat, abdominal adipose depots, skeletal intramyocellular lipids, intrahepatocellular lipids) and markers of MetSyn. An experimental intervention was then employed to examine the effect of physical activity on body fat distribution, insulin sensitivity, and haemodynamic and biochemical markers of MetSyn, and additionally to determine if the effect of exercise on parameters of MetSyn was mediated by a change in body fat patterning. Data were collected in a group of 15 obese (mean BMI Z-score 2.51 ± 0.49), prepubertal children (6 male, 9 female) aged 5.1 – 11.4 years (mean age 7.82 yrs ± 1.83). Measures included insulin sensitivity, blood biochemistry (lipid, haemostatic and adipocyte activity markers), blood pressure, two-compartment body composition by hydrometry, and nuclear magnetic resonance scanning for abdominal adipose depots, intrahepatic lipids and skeletal intramyocellular lipids. Each child’s habitual nutrition and physical activity were also ascertained using multiple-pass 24-hr diet recalls and accelerometry respectively. Data collection was conducted pre and post a 12-week physical activity intervention which consisted of cardiorespiratory activity during instructor led sessions (60 mins, twice weekly) and family led sessions (>10 mins, 4 days/wk). There is no universally accepted definition of MetSyn in childhood. The International Diabetes Federation suggests that MetSyn should not be diagnosed in children aged 6 to < 10 years. Children can be identified to be at risk of MetSyn, however, based on waist circumference ≥90th percentile and family history1,2; all subjects in this study were at risk according to these criteria. Four definitions of paediatric MetSyn previously applied to a group of young, overweight Australian children3 were used to calculate the prevalence of MetSyn in the current sample and it was found to be 27-89% at baseline and 13-80% after the experimental intervention depending upon the definition used. Acanthosis nigricans and impaired glucose tolerance (IGT) were present in one female child. Post-intervention, IGT had resolved and the child was glucose tolerant. Habitual dietary intake (energy intake and macronutrients) measured over a 3-day period pre-intervention displayed a significant positive association between fasting glucose and energy intake, as well as a significant negative association between fasting glucose and the protein component of the diet. Following the physical activity programme, energy intake was significantly positively correlated with body fat percentage (% BF). There was no difference found in dietary intake assessed prior to and following cessation of the physical activity intervention, in terms of energy or % energy from macronutrients. Habitual physical activity was not related to MetSyn diagnostic indicators. A higher level of physical fitness, estimated by predicted O2max (ml•kg-1•min-1), was significantly correlated with a lower level of diastolic blood pressure at baseline. A greater fitness level ( O2max) was moderately correlated with a lower BMI Z-score following the 12-week intervention. There was no difference between pre- and post-intervention habitual physical activity. A trend towards less sedentary time and increased light intensity activity was found, but these did not reach significance. Physical fitness level showed a trend for improvement following the intervention (P = 0.060). Anthropometrically determined body composition and body fat distribution did not change following the intervention. Radiologically determined abdominal adipose tissue depots were not significantly different post-intervention. % BF was not different when assessed with bioelectrical impedance analysis. However, % BF did reduce significantly over the 12-week intervention period when quantified by hydrometry (42.3% ± 5.0 vs 36.9% ± 8.6, P = 0.022). Adipokines, the secretory products of adipocytes displaying pleiotropic metabolic action, were investigated for their relation to lipid depots and additionally for change post-intervention. Cardiovascular (CV) disease risk was investigated by proatherogenic and protective blood lipids. When examined at baseline, fasting blood triacylglycerols (TAG) were inversely associated with basal and stimulated insulin sensitivity. Post-intervention, a higher level of HDL-C was found to be associated with greater insulin sensitivity, although this was not apparent at baseline. The relation between TAG and insulin sensitivity discovered pre-intervention was no longer evident. All other biomarkers of CV risk were not associated with body composition, glucose homeostasis, and lifestyle factors pre- and post-intervention. The effect of the physical activity intervention on indicators of haemostasis, physical fitness, blood lipids and lipoproteins, systemic inflammation, and fibrinolytic activity were analysed for change. Both systolic and diastolic blood pressure were significantly reduced following the physical activity programme. There was no significant difference found in any other measured parameter of CV risk. Log[HOMA], a surrogate index of insulin resistance, was significantly decreased post-intervention indicating reduced insulin resistance. QUICKI, a surrogate index of insulin sensitivity, was significantly improved post-intervention. The remaining indicators of insulin resistance, insulin sensitivity and β-cell function based on fasting surrogates did not significantly change over the 12-week experimental period. Dynamic insulin sensitivity and β-cell function were investigated pre- and post-intervention using paired samples t-tests. Glucose and insulin area under the curve of the OGTT were significantly reduced and whole-body insulin sensitivity index (WBISI) was significantly increased hence showing an improvement in stimulated insulin sensitivity. AUCCP/AUCglu significantly declined also indicating an improved response to oral glucose stimulation. IGI and ΔCP30/ΔG30, as markers of β-cell insulin secretion, did not change. Disposition index, the interrelationship of insulin secretion (IGI) and insulin sensitivity (WBISI), was not changed pre- and post-intervention. Hepatic insulin extraction was increased post-intervention (4.3 ± 1.2 vs 4.8 ± 1.1, P = 0.022) possibly due to greater hepatic and/or peripheral insulin sensitivity. General linear modeling (GLM) showed the improvement in whole-body insulin sensitivity discovered following the intervention was independent of % BF, abdominal adipose tissue depots, and ectopic lipid depots. Intrahepatocellular lipids (IHCL) significantly decreased after the 12-week intervention (6.99% ± 9.41 vs 5.83% ± 8.54) whilst there was no significant change in the serum markers of liver inflammation. IHCL was positively and strongly associated with total abdominal adipose tissue, intra-abdominal adipose tissue and subcutaneous abdominal adipose tissue both before and after the intervention. IHCL was positively associated with %BF measured post-intervention; this relationship almost reached significance when measured pre-intervention (P = 0.060). IHCL was not associated with insulin sensitivity either pre- or post-intervention nor with circulating lipids at either timepoint. The change in IHCL was independent of % BF and abdominal adipose tissue tested by GLM. However, there was no significant difference found in IHCL post-intervention after adjustment for insulin sensitivity (WBISI) by GLM. Prior to intervention, 10 of 15 subjects had hepatic steatosis diagnostic of non-alcoholic fatty liver disease. Eight of the 10 subjects with clinically significant hepatic steatosis had reduction of fatty infiltrate following the exercise intervention. In the whole group it was demonstrated that physical activity attenuates lipid infiltration of the liver independent of body fat. To further investigate the pathophysiology of ectopic lipid depots, biomarkers of oxidative stress and anti-oxidant status were examined in relation to IHCL. Pre-intervention, there was no association found between pro-oxidative or anti-oxidative activity and IHCL. Post-intervention, an inverse association of plasma carotenoid:cholesterol ratio with IHCL was found. Skeletal intramyocellular lipids (IMCL) measured in the right soleus were significantly increased post-intervention (2.4 ± 1.1 vs 2.6 ± 1.2, P = 0.035). There was no association between IMCL and % BF when measured pre- or post-intervention. Abdominal adipose depots were associated with IMCL at baseline and following the intervention. IMCL was not related to IHCL at either timepoint. Pre-intervention, there was a trend for a relationship between IMCL and insulin. Post-intervention, IMCL was tightly and inversely correlated with insulin sensitivity (r = -0.85 P = 0.000). Linear regression between IMCL and WBISI run pre-intervention and post-intervention found the slopes were not significantly different whereas the intercepts were highly significantly different (P = 0.001), thus, as IMCL increased there was a corresponding decrease in insulin sensitivity. GLM found the increase in IMCL was independent of % BF and abdominal adipose tissue, but was not independent of WBISI. These data indicate the greater IMCL level found post-intervention was a non-pathologic training adaptation. To further investigate the pathophysiology of ectopic lipid depots, biomarkers of oxidative stress and anti-oxidant status were examined in relation to IMCL. Pre-intervention, there was a positive association between malondialdehyde and IMCL. Post-intervention, an inverse association was found between IMCL and both plasma total carotenoids and total carotenoid:free cholesterol ratio. In summation, this study found improved metabolic health in obese, prepubertal children following a 12-week physical activity intervention without dietary intervention or intentional weight loss. Body fat and fat distribution were not prime mediators for the effect of the intervention on parameters of the Metabolic Syndrome; whereas insulin sensitivity was discovered to be a mediator of the change shown in ectopic fat depots. Causality and directionality of these fascinating relationships cannot be determined from the present study, and further research is encouraged. This thesis offers an insight into the pathogenesis of MetSyn and the use of physical activity to improve MetSyn in the setting of paediatric obesity.

In horses, a painful and often debilitating disease known as laminitis can result in impaired function and, in severe cases, euthanasia. Equine Metabolic Syndrome (EMS) is a syndrome in horses that results in development of laminitis and is characterized by the presence of general and/or regional adiposity (“cresty neck”), aberrations in blood lipid concentrations, insulin resistance (IR) and/ or hyperinsulinemia. Therapies have focused on improving the state of obesity and insulin resistance with the goal of diminishing the likelihood of laminitis development. A definitive cause for laminitis has not been established, but hyperinsulinemia and IR are likely candidates as experimental states of hyperinsulinemia have been shown to induce laminitis and improvements in insulin sensitivity and obesity have been associated with a decreased risk of laminitis development. This dissertation discusses associations between obesity and IR, as well as potential therapies for alleviating insulin resistance with the ultimate goal of decreasing the risk of developing laminitis. Therapies evaluated included chromium and magnesium, levothyroxine sodium, and metformin hydrochloride. Horses were treated with each supplement for 10 to 36 weeks, depending on the supplement tested, and physical measurements such as body weight, neck circumference, and body condition score were obtained. Throughout each study, blood concentrations of glucose, insulin, and plasma lipids were analyzed. Chromium and magnesium currently do not appear to have any effect on insulin sensitivity, whereas results of levothyroxine administration indicate therapeutic responses, as does metformin, though results indicate further work are required. Research contained in this dissertation focuses on the potential of identifying animals at risk of developing IR and laminitis through measurement of blood biomarkers such as adiponectin and glucagon-like peptide 1. Assays to measure markers included enzyme-linked immunosorbent assays, western blots, and radioimmunoassays. Glucagon-like peptide 1 currently does not appear to differ between healthy and IR animals, but protein band density of high-molecular weight adiponectin does appear to be lower in horses with IR when compared to healthy animals. There is still much to learn about IR in horses, and therapy appears to be dependent on a case by case basis.

Übergewicht und Adipositas führen zu Insulinresistenz und erhöhen deutlich das Risiko für die Entwicklung von Typ-2-Diabetes und kardiovaskulären Erkrankungen. Sowohl Adipositas als auch die Suszeptibilität gegenüber Diabetes sind zu einem erheblichen Teil genetisch determiniert. Die relevanten Risikogene, deren Interaktion mit der Umwelt, insbesondere mit Bestandteilen der Nahrung, und die Pathomechanismen, die zur Insulinresistenz und Diabetes führen, sind nicht vollständig aufgeklärt. In der vorliegenden Arbeit sollte durch Genexpressionsanalysen des weißen Fettgewebes (WAT) und der Langerhansschen Inseln die Entstehung und Progression von Adipositas und Typ-2-Diabetes untersucht werden, um relevante Pathomechanismen und neue Kandidatengene zu identifizieren. Zu diesem Zweck wurden Diät-Interventionsstudien mit NZO- und verwandten NZL-Mäusen, zwei polygenen Mausmodellen für das humane metabolische Syndrom, durchgeführt. Eine kohlenhydrathaltige Hochfett-Diät (HF: 14,6 % Fettanteil) führte in beiden Mausmodellen zu früher Adipositas, Insulinresistenz und Typ 2 Diabetes. Eine fettreduzierte Standarddiät (SD: 3,3 % Fettanteil), welche die Entstehung von Adipositas und Diabetes stark verzögert, sowie eine diabetesprotektive kohlenhydratfreie Hochfett-Diät (CHF: 30,2 % Fettanteil) dienten als Kontrolldiäten. Mit Hilfe der Microarray-Technologie wurden genomweite Expressionsprofile des WAT erstellt. Pankreatische Inseln wurden durch laserbasierte Mikropräparation (Laser Capture Microdissection; LCM) isoliert und ebenfalls hinsichtlich ihres Expressionsprofils analysiert. Differenziell exprimierte Gene wurden durch Real-Time-PCR validiert. Im WAT der NZO-Maus bewirkte die HF-Diät eine reduzierte Expression nukleärer Gene der oxidativen Phosphorylierung und von lipogenen Enzymen. Dies deutet auf eine inadäquate Fettspeicherung und -verwertung in diesen Tieren hin. Die Reduktion in der Fettspeicherung und -oxidation ist spezifisch für das adipöse NZO-Modell und konnte bei der schlanken SJL Maus nicht beobachtet werden, was auf eine mögliche Beteiligung an der Entstehung der Insulinresistenz hinweist. Zusätzlich wurde bestätigt, dass die Expansion des Fettgewebes bei der adipösen NZO-Maus eine zeitlich verzögerte Infiltration von Makrophagen in das WAT und dort eine lokale Immunantwort auslöst. Darüber hinaus wurde die Methode der LCM etabliert und zur Gewinnung hochangereicherter RNA aus den Langerhansschen Inseln eingesetzt. In erstmalig durchgeführten genomweiten Expressionsanalysen wurde zu einem frühen Zeitpunkt in der Diabetesentwicklung der Einfluss einer diabetogenen HF-Diät und einer diabetesprotektiven CHF-Diät auf das Expressionsprofil von pankreatischen Inselzellen verglichen. Im Gegensatz zum WAT bewirkt die diabetogene HF-Diät in Inselzellen einerseits, eine erhöhte Expression von nukleären Genen für die oxidative Phosphorylierung und andererseits von Genen, die mit Zellproliferation assoziiert sind. Zudem wurden 37 bereits annotierte Gene identifiziert, deren differenzielle Expression mit der Diabetesentwicklung korreliert. Das Peptidhormon Cholecystokinin (Cck, 11,8-fach erhöht durch die HF) stellt eines der am stärksten herauf regulierten Gene dar. Die hohe Anreicherung der Cck-mRNA in Inselzellen deutet auf eine bisher unbekannte Funktion des Hormons in der Regulation der Inselzellproliferation hin. Der Transkriptionsfaktor Mlxipl (ChREBP; 3,8-fach erniedrigt durch die HF) stellt in Langerhansschen Inseln eines der am stärksten herunter regulierten Gene dar. Ferner wurde ChREBP, dessen Funktion als glucoseregulierter Transkriptionsfaktor für lipogene Enzyme bislang in der Leber, aber nicht in Inselzellen nachgewiesen werden konnte, erstmals immunhistochemisch in Inselzellen detektiert. Dies deutet auf eine neue, bisher unbekannte regulatorische Funktion von ChREBP im Glucosesensor-Mechanismus der Inselzellen hin. Eine durchgeführte Korrelation der mit der Diabetesentwicklung assoziierten, differenziell exprimierten Inselzellgene mit Genvarianten aus humanen genomweiten Assoziationsstudien für Typ-2-Diabetes (WTCCC, Broad-DGI-T2D-Studie) ermöglichte die Identifizierung von 24 neuartigen Diabetes-Kandidatengenen. Die Ergebnisse der erstmals am polygenen NZO-Mausmodell durchgeführten genomweiten Expressionsuntersuchungen bestätigen bisherige Befunde aus Mausmodellen für Adipositas und Diabetes (z.B. ob/ob- und db/db-Mäuse), zeigen in einigen Fällen aber auch Unterschiede auf. Insbesondere in der oxidativen Phosphorylierung könnten die Ergebnisse relevant sein für das Verständnis der Pathogenese des polygen-bedingten humanen metabolischen Syndroms. / Overweight and obesity cause insulin resistance and increase the risk of developing type 2 diabetes and cardiovascular diseases. Both, obesity and susceptibility to diabetes, are to a major part genetically predisposed. The relevant genes, their interaction with the environment – especially with food components – and the pathomechanisms causing insulin resistance and diabetes are not fully known yet. In the present study the development and progression of obesity and type 2 diabetes should be investigated by the means of gene expression analyses of the white adipose tissue (WAT) and the islets of Langerhans to identify underlying pathomechanisms and new causative candidate genes. For this purpose diet intervention studies on NZO- and related NZL-mice – two polygenic mouse models for the human metabolic syndrome – were performed. A carbohydrate containing high fat-diet (HF: 14.6 % fat) caused early obesity, insulin resistance and type 2 diabetes in both mouse models. A fat reduced standard chow (SD: 3.3 % fat) which strongly delayed the onset of obesity and diabetes, and a diabetes protective carbohydrate free high fat-diet (CHF: 30.2 % fat) served as control diets. Using microarray technology genome wide expression profiles of the WAT were generated. Pancreatic islets were isolated by the means of laser capture microdissection (LCM) and expression profiles of them were created, too. Differentially expressed genes were validated by quantitative real time PCR. The HF-diet reduced the expression of nuclear genes of the oxidative phosphorylation and lipogenic enzymes in the WAT of the NZO-mouse. This suggests an inadequate storage and utilization of fat in these animals. This is specific for the obese NZO-model and wasn’t observed for the lean SJL-mouse, indicating a role in the development of insulin resistance. Additionally, there was proof that the enlargement of the WAT triggers a retarded infiltration of macrophages into the WAT and there a local immune response. Moreover, the LCM technique was established and used for the isolation of highly enriched RNA from islets of Langerhans. For the first time the influence of carbohydrates in a high fat-diet on the expression profile of pancreatic islets was investigated by the use of genome wide expression analyses at an early time point at the onset of diabetes. Contrary to the WAT the diabetogenic HF-diet in islets cells increased the expression of both nuclear genes coding for the oxidative phosphorylation and genes associated with cell proliferation. Furthermore 37 already annotated genes correlated with diabetes progression were identified. The peptide hormone cholecystokinin (Cck: 11.8-fold enriched by the HF-diet) is one of the most up-regulated genes. The strong enrichment of Cck-mRNA in islets suggests a previously unknown function of the hormone in the regulation of the islet cell proliferation. The transcription factor ChREBP (Mlxipl: 3.8-fold reduced by the HF-diet) is one of the most down-regulated genes in the islets of Langerhans. Moreover, ChREBP, which has been already identified as a glucose regulated transcription factor for lipogenic enzymes in the liver but not in islets of Langerhans, was detected for the first time in islet cells, using immunohistochemistry. This points to an until now unknown regulatory function of ChREBP in the glucosesensor mechanism of the islet cells. Correlation of the differentially expressed genes associated with diabetes progression with gene variants from human genome wide association studies for type 2 diabetes (WTCCC, Broad-DGI-T2D-study) made the identification of 24 new diabetes candidate genes possible. The results of the genome wide expression analyses, which were done for the first time on a polygenic mouse-model, corroborated previous results for monogenic mouse-models for obesity and diabetes (e.g. ob/ob- and db/db-mice), however also demonstrated differences in some instances. Especially the results concerning the oxidative phosphorylation could be relevant for the comprehension of the pathogenesis of the polygenic human metabolic syndrome.

This purpose of this thesis was to develop a pilot study to determine if omega-3 fatty acids and vitamin D3 will improve body weight loss and improve risk factors for Metabolic Syndrome within a weight loss program. Risk factors include obesity, hypertension, hyperglycemia, and dyslipidemia. Thirty-five men and women between 18 and 65 years of age with risk factors for Metabolic Syndrome were recruited for this study. All participants followed an energy-restricted, low glycemic-index based diet and exercise program for 16 weeks. Half of these participants received omega-3 fatty acid and vitamin D3 supplements. In those that received these supplements, it was seen that their serum 25-hydroxyvitamin D2/D3 levels and incorporation of docosahexaenoic acid and eicosapentaenoic acid into red blood cell phospholipids improved. The effect of supplementation on changes to body weight and risk factors for Metabolic Syndrome did not reach significance (p<0.05). It was however demonstrated, that an energy-restricted, low glycemic index diet with exercise was effective in inducing weight loss and improving Metabolic Syndrome risk factors with a 50% reduction in participants who had the criteria for diagnosis of Metabolic Syndrome by week 16.

BACKGROUND: The prevalence and burden of cardiovascular disease (CVD) is a concern. While CVD events will occur later in a woman’s life, modifiable risk factors for CVD occur earlier during adult years. While, there is strong evidence linking modifiable risk factors to CVD, the influence of the work environment on CVD risk is poorly understood. OBJECTIVES: The study objectives were to: 1) determine the prevalence of cardiovascular risk indicators; 2) determine the relationships between work patterns and lifestyle behaviours in female hospital workers; 3) determine the relationships between work patterns and cardiovascular risk indicators; and 4) determine the relationships between work patterns, lifestyle behaviours and cardiovascular risk while controlling for covariates. METHODS: Participants were female hospital workers (N= 466) from 2 hospital sites in Southeastern Ontario. Cardiovascular risk data were obtained through anthropometric measurements, blood sampling and self-report. Work pattern data were collected through self-report and linked with hospital administrative work data. Lifestyle behaviour data were obtained through self-report using validated questionnaires. Metabolic syndrome was classified in accordance with the National Cholesterol Education Program Adult Treatment Panel (NCEP ATP) (III) guidelines. RESULTS: Approximately 1 in 4 female participants had the metabolic syndrome, with elevated waist circumference being the most common CVD risk factor. After adjustments, the multivariate analysis found a few key significant associations between irregular work patterns, specifically extended shifts and CVD risk, specifically elevated systolic and diastolic blood pressure. However, consistent with the literature, the bivariate analyses revealed that after 6 or more years of shift work, female workers were more likely to develop the metabolic syndrome (OR 1.9, 95% CI 1.12, 3.17) and abdominally obesity (OR = 2.0, 95% CI, 1.31, 3.11). CONCLUSIONS: The findings from this study suggest that generally work patterns do not influence the development of unhealthy behaviours and cardiovascular risk factors, although a few key exceptions exist. Further research is needed to elucidate the mechanisms linking harmful and protective work pattern characteristics to CVD risk. Given the prevalence of abdominal obesity and overall CVD risk, hospital decision makers need to consider cardiovascular health within healthy workplace initiatives as the healthcare workforce is aging. / Thesis (Master, Nursing) -- Queen's University, 2009-09-24 18:39:03.718

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Thesis ((Ph.D. (Physiology))--North-West University, Potchefstroom Campus, 2010.

Objective: To compare psychological work and life stress indicators among female hospital employees in both shift work (SW) and non-shift work (NSW) positions, and determine associations with demographic and vocational factors, and indicators of cardiovascular risk (CVR). Methods: Female employees from one Southeastern Ontario acute care hospital (n=212) provided fasting blood samples, demographic and work related data, and completed a physical assessment and questionnaires. Work stress was measured with the Job Content Questionnaire and Effort-Reward Balance Index (ERI). Life stress was assessed with the Derogatis Stress Profile. Metabolic Syndrome (MS) was determined based on Interim Societies Joint Guidelines. Results: SW in comparison to NSW employees reported higher mean scores in: global ERI (.70 (SD .4) vs. .58 (SD.29) p<.05), psychological job demands (21.2 (SD 4.8) vs. 19.2 (5.7) p<.01), physical job demands (13.8 (SD 2.6) vs. 10.2 (SD 3.8), skill discretion (36.5 (SD 4.4) vs. 34.7 (SD 5.4) p<.01), lower decision authority (31.6 (SD 5.8) vs. 33.5 (SD 6.5) p<.05), and lower total life stress scores (39.2 (SD 7.3) vs. 42.1 (SD 9.4) p<.05). There were no significant differences between SW and NSW group for MS or CVR factors. MS was present among 17% of all employees, 18.5% of SW, and 15.5% of NSW. In logistic regression analysis MS occurrence was associated with chronic SW exposure of 6 or more years (AOR 5.41 (95% CI, 1.84 – 15.87), decisional authority (AOR 1.09 (95% CI, 1.00 – 1.18), skill discretion (AOR 1.13 (95% CI, 1.01 – 1.26), and depression (AOR 1.26 (95% CI 1.08 – 1.46). Conclusions: Women working in SW positions experience more psychological and physical work stress, and effort-reward imbalance. The interplay between effort and reward aspects of the work environment may significantly contribute to psychological work stress and persist with increasing age among female hospital employees regardless of SW status. Among female hospital employees SW status and psychological stress measures do not appear to have an immediate effect upon CVR, as measured by the MS, but may contribute to its development with prolonged exposure. / Thesis (Master, Nursing) -- Queen's University, 2014-04-27 21:22:11.951