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Showing 1 to 9 of 9 (0.053 seconds)Spelling suggestions: "subject:"barker ahypothesis"" "subject:"barker 1hypothesis""
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Prenatal Exposure to Maternal Cigarette Smoke and Offspring Body Mass Index: A Prospective Study of Québec ChildrenGravel, Jonathan 28 September 2011 (has links)
Concern is mounting over the increase in prevalence and severity of overweight and obesity in children worldwide. Intrauterine life has been identified as a critical period for the development of overweight or obesity and other related chronic diseases. Prenatal exposure to maternal cigarette smoke (PEMCS) has consistently emerged as an important risk factor for excess weight in the offspring and is a targetable behaviour for prevention strategies.
This study examines first the relationship between PEMCS and overweight status of children at 10 years of age and second, whether PEMCS is associated with distinct longitudinal BMI trajectories. Analyses include multivariate and multinomial logistic regression and longitudinal group based modeling methods.
PEMCS was found to be a significant risk factor for overweight in children independent of birth weight and catch-up growth. However, PEMCS was not associated with BMI trajectory membership. Our results lend support to the paradigm of in-utero excess weight prevention.
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Prenatal Exposure to Maternal Cigarette Smoke and Offspring Body Mass Index: A Prospective Study of Québec ChildrenGravel, Jonathan 28 September 2011 (has links)
Concern is mounting over the increase in prevalence and severity of overweight and obesity in children worldwide. Intrauterine life has been identified as a critical period for the development of overweight or obesity and other related chronic diseases. Prenatal exposure to maternal cigarette smoke (PEMCS) has consistently emerged as an important risk factor for excess weight in the offspring and is a targetable behaviour for prevention strategies.
This study examines first the relationship between PEMCS and overweight status of children at 10 years of age and second, whether PEMCS is associated with distinct longitudinal BMI trajectories. Analyses include multivariate and multinomial logistic regression and longitudinal group based modeling methods.
PEMCS was found to be a significant risk factor for overweight in children independent of birth weight and catch-up growth. However, PEMCS was not associated with BMI trajectory membership. Our results lend support to the paradigm of in-utero excess weight prevention.
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| 3 |
Prenatal Exposure to Maternal Cigarette Smoke and Offspring Body Mass Index: A Prospective Study of Québec ChildrenGravel, Jonathan 28 September 2011 (has links)
Concern is mounting over the increase in prevalence and severity of overweight and obesity in children worldwide. Intrauterine life has been identified as a critical period for the development of overweight or obesity and other related chronic diseases. Prenatal exposure to maternal cigarette smoke (PEMCS) has consistently emerged as an important risk factor for excess weight in the offspring and is a targetable behaviour for prevention strategies.
This study examines first the relationship between PEMCS and overweight status of children at 10 years of age and second, whether PEMCS is associated with distinct longitudinal BMI trajectories. Analyses include multivariate and multinomial logistic regression and longitudinal group based modeling methods.
PEMCS was found to be a significant risk factor for overweight in children independent of birth weight and catch-up growth. However, PEMCS was not associated with BMI trajectory membership. Our results lend support to the paradigm of in-utero excess weight prevention.
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| 4 |
Prenatal Exposure to Maternal Cigarette Smoke and Offspring Body Mass Index: A Prospective Study of Québec ChildrenGravel, Jonathan January 2011 (has links)
Concern is mounting over the increase in prevalence and severity of overweight and obesity in children worldwide. Intrauterine life has been identified as a critical period for the development of overweight or obesity and other related chronic diseases. Prenatal exposure to maternal cigarette smoke (PEMCS) has consistently emerged as an important risk factor for excess weight in the offspring and is a targetable behaviour for prevention strategies.
This study examines first the relationship between PEMCS and overweight status of children at 10 years of age and second, whether PEMCS is associated with distinct longitudinal BMI trajectories. Analyses include multivariate and multinomial logistic regression and longitudinal group based modeling methods.
PEMCS was found to be a significant risk factor for overweight in children independent of birth weight and catch-up growth. However, PEMCS was not associated with BMI trajectory membership. Our results lend support to the paradigm of in-utero excess weight prevention.
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Essays in Economics of Social Security Disability Insurance and HealthKim, Seonghoon 09 August 2013 (has links)
No description available.
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Child growth and Type 2 Diabetes Mellitus in a Queensland Aboriginal CommunityBambrick, Hilary Jane, Hilary.Bambrick@anu.edu.au January 2003 (has links)
Globally, the prevalence of Type 2 diabetes is rising. The most affected populations are those that have undergone recent and rapid transition towards a Western lifestyle, characterised by energy-dense diets and physical inactivity.¶
Two major hypotheses have attempted to explain the variation in diabetes prevalence, both between and within populations, beyond the contributions made by adult lifestyle. The thrifty genotype hypothesis proposes that some populations are genetically well adapted to surviving in a subsistence environment, and are predisposed to develop diabetes when the dietary environment changes to one that is fat and carbohydrate rich. The programming hypothesis focuses on the developmental environment, particularly on prenatal and early postnatal conditions: nutritional deprivation in utero and early postnatal life, measured by low birthweight and disrupted child growth, is proposed to alter metabolism permanently so that risk of diabetes is increased with subsequent exposure to an energy-dense diet. Both hypotheses emphasise discord between adaptation (genetic or developmental) and current environment, and both now put forward insulin resistance as a likely mechanism for predisposition.¶
Diabetes contributes significantly to morbidity and mortality among Australia’s Indigenous population. Indigenous babies are more likely to be low birthweight, and typical patterns of child growth include periods of faltering and rapid catch-up. Although there have been numerous studies in other populations, the programming hypothesis has not previously been tested in an Australian Indigenous community. The framework of the programming hypothesis is thus expanded to consider exposure of whole populations to adverse prenatal and postnatal environments, and the influence this may have on diabetes prevalence.¶
The present study took place in Cherbourg, a large Aboriginal community in southeast Queensland with a high prevalence of diabetes. Study participants were adults with diagnosed diabetes and a random sample of adults who had never been diagnosed with diabetes. Data were collected on five current risk factors for diabetes (general and central obesity, blood pressure, age and family history), in addition to fasting blood glucose levels. A lifestyle survey was also conducted. Participants’ medical records detailing weight growth from birth to five years were analysed with regard to adult diabetes risk to determine whether childhood weight and rate of weight gain were associated with subsequent diabetes. Adult lifestyle factors were
xiialso explored to determine whether variation in nutrition and physical activity was related to level of diabetes risk.¶
Approximately 20% of adults in Cherbourg have diagnosed diabetes. Prevalence may be as high as 38.5% in females and 42% in males if those who are high-risk (abnormal fasting glucose and three additional factors) are included. Among those over 40 years, total prevalence is estimated to be 51% for females and 59% for males.¶
Patterns of early childhood growth may contribute to risk of diabetes among adults. In particular, relatively rapid weight growth to five years is associated with both general and central obesity among adult women. This lends some qualified support to the programming hypothesis as catch-up growth has previously been incorporated into the model; however, although the most consistent association was found among those who gained weight more rapidly, it was also found that risk is increased among children who are heavier at any age.¶
No consistent associations were found between intrauterine growth retardation (as determined by lower than median birthweight and higher than median weight growth velocity to one and three months) and diabetes risk among women or men. A larger study sample with greater statistical power may have yielded less ambiguous results.¶
Among adults, levels of physical activity may be more important than nutritional intake in moderating diabetes risk, although features of diet, such as high intake of simple carbohydrates, may contribute to risk in the community overall, especially in the context of physical inactivity. A genetic component is not ruled out. Two additional areas which require further investigation include stress and high rates of infection, both of which are highly relevant to the study community, and may contribute to the insulin resistance syndrome.¶
Some accepted thresholds indicating increased diabetes risk may not be appropriate in this population. Given the relationship between waist circumference and other diabetes risk factors and the propensity for central fat deposition among women even with low body mass index (BMI), it is recommended that the threshold where BMI is considered a risk be lowered by 5kg/m2 for women, while no such recommendation is made for men.¶
There are a number of social barriers to better community health, including attitudes to exercise and obesity, patterns of alcohol and tobacco use and consumption of fresh foods. Some of these barriers are exacerbated by gender roles and expectations.¶
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BIRTHWEIGHT AND SUSCEPTIBILITY TO CHRONIC DISEASEIssa Al Salmi Unknown Date (has links)
The thesis examines the relationship of birthweight to risk factors and markers, such as proteinuria and glomerular filtration rate, for chronic disease in postnatal life. It made use of the Australian Diabetes, Obesity and Lifestyle Study (AusDiab). The AusDiab study is a cross sectional study where baseline data on 11,247 participants were collected in 1999-2000. Participants were recruited from a stratified sample of Australians aged ≥ 25 years, residing in 42 randomly selected urban and non-urban areas (Census Collector Districts) of the six states of Australia and the Northern Territory. The AusDiab study collected an enormous amount of clinical and laboratory data. During the 2004-05 follow-up AusDiab survey, questions about birthweight were included. Participants were asked to state their birthweight, the likely accuracy of the stated birthweight and the source of their stated birthweight. Four hundred and twelve chronic kidney disease (CKD) patients were approached, and 339 agreed to participate in the study. The patients completed the same questionnaire. Medical records were reviewed to check the diagnoses, causes of kidney trouble and SCr levels. Two control subjects, matched for gender and age, were selected for each CKD patient from participants in the AusDiab study who reported their birthweight. Among 7,157 AusDiab participants who responded to the questionnaire, 4,502 reported their birthweights, with a mean (standard deviation) of 3.4 (0.7) kg. The benefit and disadvantages of these data are discussed in chapter three. The data were analysed for the relationship between birthweight and adult body size and composition, disorders of glucose regulation, blood pressure, lipid abnormalities, cardiovascular diseases and glomerular filtration rate. Low birthweight was associated with smaller body build and lower lean mass and total body water in both females and males. In addition low birthweight was associated with central obesity and higher body fat percentage in females, even after taking into account current physical activity and socioeconomic status. Fasting plasma glucose, post load glucose and glycosylated haemoglobin were strongly and inversely correlated with birthweight. In those with low birthweight (< 2.5 kg), the risks for having impaired fasting glucose, impaired glucose tolerance, diabetes and all abnormalities combined were increased by 1.75, 2.22, 2.76 and 2.28 for females and by 1.40, 1.32, 1.98 and 1.49 for males compared to those with normal birthweight (≥ 2.5 kg), respectively. Low birthweight individuals were at higher risk for having high blood pressure ≥ 140/90 mmHg and ≥ 130/85 mmHg compared to those with normal birthweight. People with low birthweight showed a trend towards increased risk for high cholesterol (≥ 5.5 mmol/l) compared to those of normal birthweight. Females with low birthweight had increased risk for high low density lipoprotein cholesterol (≥ 3.5 mmol/l) and triglyceride levels (≥ 1.7 mmol/l) when compared to those with normal birthweight. Males with low birthweight exhibited increased risk for low levels of high density lipoprotein cholesterol (<0.9 mmol/l) than those with normal birthweight. Females with low birthweight were at least 1.39, 1.40, 2.30 and 1.47 times more likely to have angina, coronary artery disease, stroke and overall cardiovascular diseases respectively, compared to those ≥ 2.5 kg. Similarly, males with low birthweight were 1.76, 1.48, 3.34 and 1.70 times more likely to have angina, coronary artery disease, stroke and overall cardiovascular diseases compared to those ≥ 2.5 kg, respectively. The estimated glomerular filtration rate was strongly and positively associated with birthweight, with a predicted increase of 2.6 ml/min (CI 2.1, 3.2) and 3.8 (3.0, 4.5) for each kg of birthweight for females and males, respectively. The odd ratio (95% confidence interval) for low glomerular filtration rate (<61.0 ml/min for female and < 87.4 male) in people of low birthweight compared with those of normal birthweight was 2.04 (1.45, 2.88) for female and 3.4 (2.11, 5.36) for male. One hundred and eighty-nineCKD patients reported their birthweight; 106 were male. Their age was 60.3(15) years. Their birthweight was 3.27 (0.62) kg, vs 3.46 (0.6) kg for their AusDiab controls, p<0.001 and the proportions with birthweight<2.5 kg were 12.17% and 4.44%, p<0.001. Among CKD patients, 22.8%, 21.7%, 18% and 37.6% were in CKD stages 2, 3, 4 and 5 respectively. Birthweights by CKD stage and their AusDiab controls were as follows: 3.38 (0.52) vs 3.49 (0.52), p=0.251 for CKD2; 3.28 (0.54) vs 3.44 (0.54), p=0.121 for CKD3; 3.19 (0.72) vs 3.43 (0.56), p= 0.112 for CKD4 and 3.09 (0.65) vs 3.47 (0.67), p<0.001 for CKD5. The results demonstrate that in an affluent Western country with a good adult health profile, low birthweight people were predisposed to higher rates of glycaemic dysregulation, high blood pressure, dyslipidaemia, cardiovascular diseases and lower glomerular filtration rate in adult life. In all instances it would be prudent to adopt policies of intensified whole of life surveillance of lower birthweight people, anticipating this risk. The general public awareness of the effect of low birthweight on development of chronic diseases in later life is of vital importance. The general public, in addition to the awareness of people in medical practice of the role of low birthweight, will lead to a better management of this group of our population that is increasingly surviving into adulthood.
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BIRTHWEIGHT AND SUSCEPTIBILITY TO CHRONIC DISEASEIssa Al Salmi Unknown Date (has links)
The thesis examines the relationship of birthweight to risk factors and markers, such as proteinuria and glomerular filtration rate, for chronic disease in postnatal life. It made use of the Australian Diabetes, Obesity and Lifestyle Study (AusDiab). The AusDiab study is a cross sectional study where baseline data on 11,247 participants were collected in 1999-2000. Participants were recruited from a stratified sample of Australians aged ≥ 25 years, residing in 42 randomly selected urban and non-urban areas (Census Collector Districts) of the six states of Australia and the Northern Territory. The AusDiab study collected an enormous amount of clinical and laboratory data. During the 2004-05 follow-up AusDiab survey, questions about birthweight were included. Participants were asked to state their birthweight, the likely accuracy of the stated birthweight and the source of their stated birthweight. Four hundred and twelve chronic kidney disease (CKD) patients were approached, and 339 agreed to participate in the study. The patients completed the same questionnaire. Medical records were reviewed to check the diagnoses, causes of kidney trouble and SCr levels. Two control subjects, matched for gender and age, were selected for each CKD patient from participants in the AusDiab study who reported their birthweight. Among 7,157 AusDiab participants who responded to the questionnaire, 4,502 reported their birthweights, with a mean (standard deviation) of 3.4 (0.7) kg. The benefit and disadvantages of these data are discussed in chapter three. The data were analysed for the relationship between birthweight and adult body size and composition, disorders of glucose regulation, blood pressure, lipid abnormalities, cardiovascular diseases and glomerular filtration rate. Low birthweight was associated with smaller body build and lower lean mass and total body water in both females and males. In addition low birthweight was associated with central obesity and higher body fat percentage in females, even after taking into account current physical activity and socioeconomic status. Fasting plasma glucose, post load glucose and glycosylated haemoglobin were strongly and inversely correlated with birthweight. In those with low birthweight (< 2.5 kg), the risks for having impaired fasting glucose, impaired glucose tolerance, diabetes and all abnormalities combined were increased by 1.75, 2.22, 2.76 and 2.28 for females and by 1.40, 1.32, 1.98 and 1.49 for males compared to those with normal birthweight (≥ 2.5 kg), respectively. Low birthweight individuals were at higher risk for having high blood pressure ≥ 140/90 mmHg and ≥ 130/85 mmHg compared to those with normal birthweight. People with low birthweight showed a trend towards increased risk for high cholesterol (≥ 5.5 mmol/l) compared to those of normal birthweight. Females with low birthweight had increased risk for high low density lipoprotein cholesterol (≥ 3.5 mmol/l) and triglyceride levels (≥ 1.7 mmol/l) when compared to those with normal birthweight. Males with low birthweight exhibited increased risk for low levels of high density lipoprotein cholesterol (<0.9 mmol/l) than those with normal birthweight. Females with low birthweight were at least 1.39, 1.40, 2.30 and 1.47 times more likely to have angina, coronary artery disease, stroke and overall cardiovascular diseases respectively, compared to those ≥ 2.5 kg. Similarly, males with low birthweight were 1.76, 1.48, 3.34 and 1.70 times more likely to have angina, coronary artery disease, stroke and overall cardiovascular diseases compared to those ≥ 2.5 kg, respectively. The estimated glomerular filtration rate was strongly and positively associated with birthweight, with a predicted increase of 2.6 ml/min (CI 2.1, 3.2) and 3.8 (3.0, 4.5) for each kg of birthweight for females and males, respectively. The odd ratio (95% confidence interval) for low glomerular filtration rate (<61.0 ml/min for female and < 87.4 male) in people of low birthweight compared with those of normal birthweight was 2.04 (1.45, 2.88) for female and 3.4 (2.11, 5.36) for male. One hundred and eighty-nineCKD patients reported their birthweight; 106 were male. Their age was 60.3(15) years. Their birthweight was 3.27 (0.62) kg, vs 3.46 (0.6) kg for their AusDiab controls, p<0.001 and the proportions with birthweight<2.5 kg were 12.17% and 4.44%, p<0.001. Among CKD patients, 22.8%, 21.7%, 18% and 37.6% were in CKD stages 2, 3, 4 and 5 respectively. Birthweights by CKD stage and their AusDiab controls were as follows: 3.38 (0.52) vs 3.49 (0.52), p=0.251 for CKD2; 3.28 (0.54) vs 3.44 (0.54), p=0.121 for CKD3; 3.19 (0.72) vs 3.43 (0.56), p= 0.112 for CKD4 and 3.09 (0.65) vs 3.47 (0.67), p<0.001 for CKD5. The results demonstrate that in an affluent Western country with a good adult health profile, low birthweight people were predisposed to higher rates of glycaemic dysregulation, high blood pressure, dyslipidaemia, cardiovascular diseases and lower glomerular filtration rate in adult life. In all instances it would be prudent to adopt policies of intensified whole of life surveillance of lower birthweight people, anticipating this risk. The general public awareness of the effect of low birthweight on development of chronic diseases in later life is of vital importance. The general public, in addition to the awareness of people in medical practice of the role of low birthweight, will lead to a better management of this group of our population that is increasingly surviving into adulthood.
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| 9 |
BIRTHWEIGHT AND SUSCEPTIBILITY TO CHRONIC DISEASEIssa Al Salmi Unknown Date (has links)
The thesis examines the relationship of birthweight to risk factors and markers, such as proteinuria and glomerular filtration rate, for chronic disease in postnatal life. It made use of the Australian Diabetes, Obesity and Lifestyle Study (AusDiab). The AusDiab study is a cross sectional study where baseline data on 11,247 participants were collected in 1999-2000. Participants were recruited from a stratified sample of Australians aged ≥ 25 years, residing in 42 randomly selected urban and non-urban areas (Census Collector Districts) of the six states of Australia and the Northern Territory. The AusDiab study collected an enormous amount of clinical and laboratory data. During the 2004-05 follow-up AusDiab survey, questions about birthweight were included. Participants were asked to state their birthweight, the likely accuracy of the stated birthweight and the source of their stated birthweight. Four hundred and twelve chronic kidney disease (CKD) patients were approached, and 339 agreed to participate in the study. The patients completed the same questionnaire. Medical records were reviewed to check the diagnoses, causes of kidney trouble and SCr levels. Two control subjects, matched for gender and age, were selected for each CKD patient from participants in the AusDiab study who reported their birthweight. Among 7,157 AusDiab participants who responded to the questionnaire, 4,502 reported their birthweights, with a mean (standard deviation) of 3.4 (0.7) kg. The benefit and disadvantages of these data are discussed in chapter three. The data were analysed for the relationship between birthweight and adult body size and composition, disorders of glucose regulation, blood pressure, lipid abnormalities, cardiovascular diseases and glomerular filtration rate. Low birthweight was associated with smaller body build and lower lean mass and total body water in both females and males. In addition low birthweight was associated with central obesity and higher body fat percentage in females, even after taking into account current physical activity and socioeconomic status. Fasting plasma glucose, post load glucose and glycosylated haemoglobin were strongly and inversely correlated with birthweight. In those with low birthweight (< 2.5 kg), the risks for having impaired fasting glucose, impaired glucose tolerance, diabetes and all abnormalities combined were increased by 1.75, 2.22, 2.76 and 2.28 for females and by 1.40, 1.32, 1.98 and 1.49 for males compared to those with normal birthweight (≥ 2.5 kg), respectively. Low birthweight individuals were at higher risk for having high blood pressure ≥ 140/90 mmHg and ≥ 130/85 mmHg compared to those with normal birthweight. People with low birthweight showed a trend towards increased risk for high cholesterol (≥ 5.5 mmol/l) compared to those of normal birthweight. Females with low birthweight had increased risk for high low density lipoprotein cholesterol (≥ 3.5 mmol/l) and triglyceride levels (≥ 1.7 mmol/l) when compared to those with normal birthweight. Males with low birthweight exhibited increased risk for low levels of high density lipoprotein cholesterol (<0.9 mmol/l) than those with normal birthweight. Females with low birthweight were at least 1.39, 1.40, 2.30 and 1.47 times more likely to have angina, coronary artery disease, stroke and overall cardiovascular diseases respectively, compared to those ≥ 2.5 kg. Similarly, males with low birthweight were 1.76, 1.48, 3.34 and 1.70 times more likely to have angina, coronary artery disease, stroke and overall cardiovascular diseases compared to those ≥ 2.5 kg, respectively. The estimated glomerular filtration rate was strongly and positively associated with birthweight, with a predicted increase of 2.6 ml/min (CI 2.1, 3.2) and 3.8 (3.0, 4.5) for each kg of birthweight for females and males, respectively. The odd ratio (95% confidence interval) for low glomerular filtration rate (<61.0 ml/min for female and < 87.4 male) in people of low birthweight compared with those of normal birthweight was 2.04 (1.45, 2.88) for female and 3.4 (2.11, 5.36) for male. One hundred and eighty-nineCKD patients reported their birthweight; 106 were male. Their age was 60.3(15) years. Their birthweight was 3.27 (0.62) kg, vs 3.46 (0.6) kg for their AusDiab controls, p<0.001 and the proportions with birthweight<2.5 kg were 12.17% and 4.44%, p<0.001. Among CKD patients, 22.8%, 21.7%, 18% and 37.6% were in CKD stages 2, 3, 4 and 5 respectively. Birthweights by CKD stage and their AusDiab controls were as follows: 3.38 (0.52) vs 3.49 (0.52), p=0.251 for CKD2; 3.28 (0.54) vs 3.44 (0.54), p=0.121 for CKD3; 3.19 (0.72) vs 3.43 (0.56), p= 0.112 for CKD4 and 3.09 (0.65) vs 3.47 (0.67), p<0.001 for CKD5. The results demonstrate that in an affluent Western country with a good adult health profile, low birthweight people were predisposed to higher rates of glycaemic dysregulation, high blood pressure, dyslipidaemia, cardiovascular diseases and lower glomerular filtration rate in adult life. In all instances it would be prudent to adopt policies of intensified whole of life surveillance of lower birthweight people, anticipating this risk. The general public awareness of the effect of low birthweight on development of chronic diseases in later life is of vital importance. The general public, in addition to the awareness of people in medical practice of the role of low birthweight, will lead to a better management of this group of our population that is increasingly surviving into adulthood.
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