Active clinical trials for "Weight Loss"

Studies have shown that patients who weigh more at the time of cancer diagnosis may be at increased risk of complications from surgery, fatigue, poor body image and other problems. Some research suggests that losing weight after cancer diagnosis can lead to improvements in these problems, as well as having other potential benefits for cancer survivors. Programs that reduce calories and increase exercise have been shown to help cancer survivors lose weight, but more research is needed to develop and test weight loss programs in cancer survivors. This study is designed to look at the ability of a 15-week diet and exercise program to help cancer survivors lose weight. The investigator will look at changes in weight, body composition, quality of life, fatigue, body image as well as diet and exercise patterns, to see if this program can help men and women feel better and live healthier lives after cancer diagnosis.

The aims of this project are to determine if dietary supplementation with NOPE-EGCG (PhosphoLeantm, 30mg NOPE+20mg EGCG per capsule) can: rescue striatal function, increase adherence to a diet, reduce weight-gain after a diet, improve performance on impulsivity, go/no-go tasks, and negative outcome learning, and shift fat and sweet preference in overweight/obese human subjects Secondary hypotheses: Baseline brain; perceptual and cognitive measures will be associated with diet, insulin sensitivity and may vary with genotype (TaqA1 1A polymorphism).

A. BACKGROUND Accumulation of fat in the liver due to non-alcoholic causes (NAFLD) is associated with hepatic insulin resistance, which impairs the ability of insulin to inhibit the production of glucose and VLDL . This leads to increases in serum glucose, insulin and triglyceride concentrations as well as hyperinsulinemia. Recent epidemiologic studies have shown that a major reason for the metabolic syndrome as well as the accompanying increased risk of cardiovascular disease and type 2 diabetes is overconsumption of simple sugars. The investigators have recently shown that overeating simple sugars (1000 extra calories/day, "CANDY" diet) increases liver fat content by 30% within 3 weeks (4), and recapitulates features of the metabolic syndrome such as hypertriglyceridemia and a low HDL cholesterol concentration. The fatty acids in intrahepatocellular triglycerides may originate from peripheral lipolysis, de novo lipogenesis, uptake of chylomicron remnants by the liver and from hepatic uptake of fatty acids released during intravascular hydrolysis of triglyceride-rich lipoproteins (the spillover pathway). A classic study using stable isotope methodology by the group of Elisabeth Parks showed that in subjects with NAFLD, the excess intrahepatocellular triglycerides originate from peripheral lipolysis and de novo lipogenesis. It is well-established that ingestion of a high carbohydrate as compared to high fat diet stimulates de novo lipogenesis in humans. Meta-analyses comparing isocaloric high fat and high carbohydrate diets have shown that high carbohydrate but not high fat diets increase increase serum triglycerides and lower HDL cholesterol. Since hypertriglyceridemia results from overproduction of VLDL from the liver, these data suggest the composition of the diet influences hepatic lipid metabolism. Whether this is because overfeeding fat leads to preferential deposition of fat in adipose tissue while high carbohydrate diets induce a relative greater increase in liver fat is unknown. There are no previous studies comparing effects of chronic overfeeding of fat as compared to carbohydrate on liver fat or and the sources of intrahepatic fatty acids. A common polymorphism in PNPLA3 at rs738409 (adiponutrin) gene is associated with a markedly increase liver fat content. This finding has been replicated in at least 20 studies across the world. The investigators have shown that PNPLA3 is regulated by the carbohydrate response element binding protein 1. Mice overexpressing the human I148M PNPLA3 variant in the liver exhibit an increase in liver triglycerides and cholesteryl esters on a high sucrose but not high fat diet. These data suggest that overfeeding a high carbohydrate as compared to a high fat diet may increase liver fat more in subjects carrying the I148M allele than in non-carriers. B. HYPOTHESIS The investigators hypothesize that overfeeding a high fat as compared to an isocaloric high carbohydrate diet influences the source of intrahepatocellular triglycerides. During a high fat diet, relatively more of intrahepatocellular triglycerides originate from peripheral lipolysis and less from DNL than during a high carbohydrate diet in the face of a similar increase in liver fat. It is also possible given the lack of previous overfeeding data comparing 2 different overfeeding diets that the high fat diet induces a smaller increase in liver fat than a high carbohydrate diet even in the face of an identical increase in caloric intake because a greater fraction of ingested fat is channeled to adipose tissue than the liver. The investigators also hypothesize that liver fat may increase more in carriers than non-carriers of the I148M variant in PNPLA3 during a high carbohydrate than a high fat diet. C. SPECIFIC AIMS The investigators wish to randomize, using the method of minimization (considers baseline age, BMI, gender, liver fat, PNPLA3 genotype) 40 non-diabetic subjects with NAFLD as determined by the non-invasive score developed in our laboratory or previous knowledge of liver fat content based on MRS to overeat either a high carbohydrate or high fat diet (1000 extra calories per day) for 3 weeks. Before and after the overfeeding diets, will measure liver fat content by 1H-MRS and the rate of adipose tissue lipolysis using doubly labeled water (DDW) and [1,1,2,3,3-2H5] glycerol as described in detail below. The investigators also wish to characterize glucose, insulin, fatty acid and triacylglyceride profiles before and while on the experimental diet. An adipose tissue biopsy is taken to determine whether expression of genes involved in lipogenesis or lipolysis, or those involved in adipose tissue inflammation change in response to overfeeding, and for measurement of LPL activity. After overfeeding, both groups will undergo weight loss to restore normal weight as described in our recent study. The metabolic study is repeated after weight loss.

Before and during bariatric surgery patients are given oral and i.v. midazolam, respectively and blood samples are drawn to establish midazolam time-concentration profiles. After 0.5-2 years, and substantial weight loss, oral and i.v. midazolam are administered once more and blood samples are taken again.

The purpose of this study is to find out the impact of improving diabetes control through weight reduction and lifestyle changes on a common diabetes complication called peripheral neuropathy.

Aims: We evaluate the efficacy of the "Active Body Control (ABC) Program" for weight reduction in patients with metabolic syndrome. Methods: The ABC program combines telemonitoring of the physical activity with a low-calorie diet also preferring carbohydrates with low glycemic indexes. In this 12-month, randomized, clinical trial 60 patients will be treated according to the ABC program and 60 control patients will receive standard therapy.

By doing this study, researchers hope to learn whether a person's motivation for food is different after he or she loses weight, and if imaging techniques such as fMRI can be used to predict whether the person will maintain that weight loss over time.

The main aim of this study is to analyze and report the preliminary and intermediate term outcomes after laparoscopic revision Roux-en-Y gastric bypass surgery for weight recidivism. The foremost outcome measurements are 1) Fat loss mainly measured as weight loss and expressed as trends in BMI, %EWL, and/or %EBL; 2) Trend in Comorbidity status; and 3) Patient satisfaction and Health-Related Quality of Life "HR-QoL" measured by a standardized, non-validated subjective satisfaction questionnaire and the validated, disease-specific, Moorehead-Ardelt II QoL questionnaires, respectively; 4) Morbidity & Mortality including nutritional status and metabolic complications. Consequently, secondary objectives of this study are 1) to assess failure rate defined as percentage of excess weight loss < 50% , lowest BMI >35 for morbidly obese (MO) or >40 for superobese (SO), and/or lack of resolution/improvement of major comorbidities at the point in time when assessing preliminary and intermediate results after the surgery under analysis. 2) To evaluate the metabolic and nutritional status by measurements of particular clinical and biochemical parameters. This research is in line with the most current provocative new ideas and recent high impact publications. To the best of our knowledge, this is the very first outcome study of revisional malabsorptive distal gastric bypass surgery by laparoscopy with diverse revisional strategies such as revisional gastroplasty, revisional Fobi-Capella, revisional Adjustable Gastric Band, conversion to distal, and conversion to very, very long limb gastric bypass. Previously, several studies have addressed conversion to malabsorptive gastric bypass after a failed primary proximal gastric bypass but none has addressed the failed distal gastric bypass nor the adequate balance between increasing restriction and malabsorption for decreasing the risk of protein-calorie malnutrition.

This project is a prospective observational study that will involve the participation of 25 volunteers that qualify for having knee osteoarthritis, are going to be having gastric bypass surgery and are willing to participate in this study which is designed to last up to two years. Potential candidates will be interviewed using a standard set of questions related to the study

The purpose of this study, then, is to search existing clinic and hospital records for answers to the following two questions: (1) Do pregnant women who are at least 37 weeks gestation and who have an increase in urubilinogen on urine dipstick at a prenatal appointment have a statistically significant shorter average time before going into active labor than their negative counterparts? (2) Do pregnant women who are at least 37 weeks gestation and who show a modest weight loss between two prenatal appointments have a statistically significant shorter average time before going into active labor than their counterparts who did not lose weight?