Current Obesity Epidemic (current + obesity_epidemic)

Distribution by Scientific Domains


Selected Abstracts


Obesity and lifestyle risk factors for gastroesophageal reflux disease, Barrett esophagus and esophageal adenocarcinoma

DISEASES OF THE ESOPHAGUS, Issue 5 2006
P. J. Veugelers
SUMMARY., The aim of this study was to examine the association of obesity with esophageal adenocarcinoma, and with the precursor lesions Barrett esophagus and gastroesophageal reflux disease (GERD). This case-control study included cases with GERD (n = 142), Barrett esophagus (n = 130), and esophageal adenocarcinoma (n = 57). Controls comprised 102 asymptomatic individuals. Using logistic regression methods, we compared obesity rates between cases and controls adjusting for differences in age, gender, and lifestyle risk factors. Relative to normal weight, obese individuals were at increased risk for esophageal adenocarcinoma (Odds Ratio [OR] 4.67, 95% Confidence Interval [CI] 1.27,17.9). Diets high in vitamin C were associated with a lower risk for GERD (OR 0.40, 95% CI 0.19,0.87), Barrett esophagus (OR 0.44, 95% CI 0.20,0.98), and esophageal adenocarcinoma (OR 0.21, 95% CI 0.06,0.77). For the more established risk factors, we confirmed that smoking was a significant risk factor for esophageal adenocarcinoma, and that increased liquor consumption was associated with GERD and Barrett esophagus. In light of the current obesity epidemic, esophageal adenocarcinoma incidence rates are expected to continue to increase. Successful promotion of healthy body weight and diets high in vitamin C may substantially reduce the incidence of this disease. [source]


Our children and the metabolic syndrome

DRUG DEVELOPMENT RESEARCH, Issue 7 2006
Jean-Claude Desmangles
Abstract The metabolic syndrome is a cluster of metabolic disturbances that result in an increased risk of type 2 diabetes and cardiovascular disease in adults. Despite the lack of a uniform definition of the syndrome for children, several studies have reported an overall prevalence of 3 to 4% among children. Among obese adolescents, the prevalence can be as high as 30 to 50%. Besides insulin resistance and obesity, the intrauterine environment and genetic factors also seem to play a role in the pathogenesis of the syndrome in children. In view of the current obesity epidemic and since an increasing amount of evidence shows that obesity during adolescence is significantly associated with insulin resistance, abnormal serum lipid levels, and elevated blood pressure during adulthood, there is a great need for a clear definition, for the development of screening guidelines, and for appropriate prevention and treatment strategies for the metabolic syndrome in the pediatric population. Drug Dev. Res. 67:602,606, 2006. 2006 Wiley-Liss, Inc. [source]


Childhood sexual abuse and obesity

OBESITY REVIEWS, Issue 3 2004
T. B. Gustafson
Summary The causes of the current obesity epidemic are multifactorial and include genetic, environmental, and individual factors. One potential risk factor may be the experience of childhood sexual abuse. Childhood sexual abuse is remarkably common and is thought to affect up to one-third of women and one-eighth of men. A history of childhood sexual abuse is associated with numerous psychological sequelae including depression, anxiety, substance abuse, somatization, and eating disorders. Relatively few studies have examined the relationship between childhood sexual abuse and adult obesity. These studies suggest at least a modest relationship between the two. Potential explanations for the relationship have focused on the role of disordered eating, particularly binge eating, as well as the possible ,adaptive function' of obesity in childhood sexual abuse survivors. Nevertheless, additional research on the relationship between childhood sexual abuse and obesity is clearly needed, not only to address the outstanding empirical issues but also to guide clinical care. [source]


Social stress, visceral obesity, and coronary artery atherosclerosis: product of a primate adaptation

AMERICAN JOURNAL OF PRIMATOLOGY, Issue 9 2009
Carol A. Shively
Abstract Abdominal obesity is prevalent and often accompanied by an array of metabolic perturbations including elevated blood pressure, dyslipidemia, impaired glucose tolerance or insulin resistance, a prothrombotic state, and a proinflammatory state, together referred to as the metabolic syndrome. The metabolic syndrome greatly increases coronary heart disease (CHD) risk. Social stress also increases CHD although the mechanisms through which this occurs are not completely understood. Chronic stress may result in sustained glucocorticoid production, which is thought to promote visceral obesity. Thus, one hypothesis is that social stress may cause visceral fat deposition and the metabolic syndrome, which, in turn increases CHD. CHD is caused by coronary artery atherosclerosis (CAA) and its sequelae. Cynomolgus monkeys (Macaca fascicularis) are a well-established models of CAA. Social subordination may be stressful to cynomolgus monkeys and result in hypercortisolemia and exacerbated CAA in females. Herein is reviewed a body of literature which suggests that social stress increases visceral fat deposition in cynomolgus monkeys, that subordinate females are more likely than dominants to have visceral obesity, that females with visceral obesity have behavioral and physiological characteristics consistent with a stressed state, and that females with high ratios of visceral to subcutaneous abdominal fat develop more CAA. While these relationships have been most extensively studied in cynomolgus macaques, obesity-related metabolic disturbances are also observed in other primate species. Taken together, these observations support the view that the current obesity epidemic is the result of a primate adaptation involving the coevolution with encephalization of elaborate physiological systems to protect against starvation and defend stored body fat in order to feed a large and metabolically demanding brain. Social stress may be engaging these same physiological systems, increasing the visceral deposition of fat and its sequelae, which increase CHD risk. Am. J. Primatol. 71:742,751, 2009. 2009 Wiley-Liss, Inc. [source]