View clinical trials related to Body Composition.
Filter by:The investigators primary objective is to evaluate the effect of a 6 month (3 days/wk) supervised, progressive RT program with increased daily milk intake in untrained adolescents on measures of body composition and cardiovascular risk factors. The investigators hypothesize that milk supplementation will produce significantly greater favorable changes in all body composition measures compared with RT + carbohydrate and control.
EDUFIT is a group-Randomized Controlled Trial specifically designed to enhance physical fitness and other health-related factors in a school setting in adolescents.
The purpose of the study is to examine how a naturally occurring fat found in meats, such as beef and lamb and milk, called conjugated linoleic acid (CLA), will affect your body weight and body fat content, blood fat levels, as well as selected safety parameters. The CLA will be supplemented in an oil form and will be added to solid foods as provided by the metabolic kitchen at the Richardson Centre for Functional Foods and Nutraceuticals (RCFFN).
A key factor in the determination of body composition over the lifecourse is fat accumulation during childhood. Periods of life associated with the greatest changes in organ development and growth, i.e. early childhood, have the most significant effect on body composition, energy balance, and metabolism. Early childhood (age 3 to 7 years) represents a critical transition for the basis of adaptability in body composition, due to the rapid growth and development that occurs. Plausibly the phenotype underlying obesity and related health risk may be determined by body composition during this critical period. Our previous research in children has consistently indicated that HA children accumulate greater amounts of fat, particularly in the intra-abdominal compartment, even at similar a BMI, and lower bone mineral content relative to EA children. The reason for these differences in body composition over the lifecourse is not clear. Racial/ethnic differences in risk factors for health, including 'thriftiness' in body fat accumulation are often evident before the age of 7, suggesting that the racial/ethnic differences in energy utilization and subsequent fat storage may be accounted for by genetic make-up, the environment (e.g. diet), or an interaction of the two. The physiologic or behavioral process(es) that cause(s) certain children to take a trajectory towards obesity while others accrue less fat is not known. However, the economic decision of fuel utilization is a physiologic trait enabling the body to choose between shuttling 'energy' towards accrual of a particular tissue (e.g. bone vs. fat) and this trait likely has a genetic component. This genetic component may be embedded in fat storage capacity evolved from gene by environment interactions that promote thrift, particularly conserved in some populations. Although genetic background plays a role, it not known whether there is a relationship between genetic background, known candidate genes or candidate pathways and environmental contributors (e.g. diet) that impact body composition trajectory. Of central importance to our understanding of early fat mass accumulation in health disparities are the mechanisms that lead to chronic disease progression. It is likely that variations within candidate genes may have a differential impact on individuals based on their genetic background. It is also probable that body composition is influenced by many genes, often within the same metabolic pathways, with small individual effects. These genes may not be significantly associated individually, but when examined as a unit (in a candidate pathway or gene-gene interaction framework) the association becomes significant. Further, children's early environmental exposures (e.g. diet) may interact with both genetic background and variations in candidate genes along resulting in alterations in body composition that predispose HA to excess fat accumulation throughout the lifecourse. To that end, the following specific aims will be evaluated: Aim 1. To examine the associations between genetic admixture and body composition in children aged 3-7 years after controlling for dietary intake. 1. Hypothesis 1.1: There is a direct association between Amerindian admixture and fat mass and in inverse association between Amerindian admixture and bone mass. 2. Hypothesis 1.2: There is a direct association between energy intake and fat accumulation and the relationship will be particularly evident in individuals with a greater proportion of Amerindian admixture. Aim 2. To examine the associations between genetic admixture and bone marrow fat in children aged 3-7 years after controlling for dietary intake. 1. Hypothesis 2.1: There is a direct association between Amerindian admixture and bone marrow fat. 2. Hypothesis 2.2: There is a direct association between energy intake and fat accumulation in bone marrow and the relationship will be particularly evident in individuals with a greater proportion of Amerindian admixture. Aim 3. To examine the relationship between variation in candidate genes and pathways and Amerindian admixture controlling for dietary intake. a. Hypothesis 3.1: Amerindian admixture will be associated with variations in candidate genes and pathways known to be associated with fat accumulation.
The objective of this trial is to examine the long-term effects of a diet low in carbohydrates, as compared to one low in fat, on cardiovascular disease risk factors, including blood pressure (BP), body weight and composition, serum lipids, plasma glucose, insulin, adipocytokines (adiponectin, leptin, resistin), and C-reactive protein (CRP) among obese adults. The investigators will test the following hypotheses: Hypothesis 1: Compared to a low fat diet, a diet low in carbohydrates will reduce systolic and diastolic BP over 12 months; Hypothesis 2: Compared to a low fat diet, a diet low in carbohydrates will reduce body weight, total percent body fat, and waist circumference over 12 months; Hypothesis 3: Compared to a low fat diet, a diet low in carbohydrates will reduce serum levels of LDL-cholesterol and triglycerides and increase serum levels of HDL-cholesterol over 12 months; Hypothesis 4: Compared to a low fat diet, a diet low in carbohydrates will reduce plasma levels of glucose and insulin levels over 12 months; and Hypothesis 5: Compared to a low fat diet, a diet low in carbohydrates will reduce plasma levels of leptin, resistin, and CRP and increase plasma levels of adiponectin over 12 months.
This project aims to a) evaluate the effects of haloperidol, olanzapine, and risperidone in combination with valproate on insulin secretion and insulin actions, b) evaluate medication effects on abdominal fat, total body fat and total fat-free mass, and c) evaluate treatment effects on glucose tolerance, lipid profiles, and plasma levels of leptin, adiponectin, ghrelin and C-reactive protein. Hypotheses will be evaluated by measuring 1) insulin action and secretion using frequently sampled intravenous glucose tolerance tests, 2) body composition using dual energy x-ray absorptiometry, magnetic resonance scans, and anthropomorphic measurements, and 3) changes in hormone levels and lipid profiles. The aims will be addressed in non-diabetic schizophrenia patients chronically treated with haloperidol, olanzapine or risperidone who will have valproate added to their treatment. Relevant data is critically needed to target basic research, identify long-term cardiovascular risks, and plan therapeutic interventions.
Impact of resistance training in prepubertal children with obesity focusing mostly in changes in body composition and markers of insulin resistance. Hypothesis is that this will show positive changes in this randomized controlled trial.
It has been proposed that a higher cut off for BMI (body mass index) is to be used in Maori to define overweight and obesity. However, no one has assessed the prevalence of co-morbid conditions associated with BMI. It is well known that Maori are at greater risk of diabetes and cardiovascular disease compared to non-Maori and a delay in the identification of those who are overweight and obese may be detrimental for Maori. We will assess BMI, other measures of adiposity and prevalence of co-morbid conditions with a comparison with a similar matched non-Maori population.