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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Gastrointestinal malignancies may be associated with obesity, defined specifically by increased body-mass index, and based largely on environmental factors rather than genetics. In particular, there seems to be a definite increase in the incidence of both oesophageal and colorectal cancer. Mechanisms associated with obesity include a particular metabolic state characterized by hyperinsulinemia, or insulin resistance, along with elevated serum leptin. Leptin is derived from adipocytes and appears to play a role in the regulation of ghrelin, a peptide derived from the stomach and small intestine that stimulates appetite and weight gain. In addition to these metabolic changes, there are other anatomical alterations that may indirectly predispose to cancer, including the predisposition of obesity to gastroesophageal reflux and, possibly, oesophageal cancer. Other mechanisms may involve adipocyte-derived cytokines, or adipokines, that may serve as signalling devices in the pathogenesis of cancer. Finally, pharmacologic and surgical avenues available for treatment of obesity, including lipase inhibitors and gastric or jejuno-ileal bypass procedures may set the stage for subsequent gastric or intestinal tract cancer.
Best Pract Res Clin Gastroenterol 2004 Dec
PMID:Risk of gastrointestinal malignancies and mechanisms of cancer development with obesity and its treatment. 1556 45

Childhood obesity is prevalent and linked to the development of Type 2 diabetes mellitus (DM) and poor bone health. Some PUFA enhance bone mass and thus may improve bone health in obese children. The study objective was to determine the effects of dietary (n-6) compared with (n-3) essential PUFA and long-chain PUFA (LCPUFA) on bone in an obese and insulin-resistant state. Male fa/fa (n = 48) and lean Zucker rats (n = 48) were fed diets containing safflower oil [SO, high (n-6) PUFA], flaxseed oil [FXO, high (n-3) PUFA], or menhaden oil [MO, high (n-3) LCPUFA] for 9 wk. Measurements included the following: femur bone area (BA), mineral content (BMC), density (BMD), morphometry and ex vivo release of prostaglandin E(2) (PGE(2)); plasma osteocalcin and C-terminal telopeptides of type I collagen. Differences among groups were detected using 2-way ANOVA. Genotype effects in the fa/fa rats included lower femoral weight, length, BA, and BMC, as well as femoral head and proximal epiphysis widths compared with the lean rats, but BMD was not affected. Femur BA, BMC, and BMD did not differ among the dietary groups, but diaphysis width was elevated in the MO group and PGE(2) release was reduced by the FXO and MO diets. No genotype x diet interactions were observed. These data indicate that the fa/fa Zucker rat is at risk for low bone mass and that dietary (n-3) FA effectively reduce PGE(2) release. Whether reduced PGE(2) will support optimal peak bone mass during childhood and conserve bone mass with aging warrants investigation.
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PMID:(n-3) fatty acids reduce the release of prostaglandin E2 from bone but do not affect bone mass in obese (fa/fa) and lean Zucker rats. 1573 84

As many as 90 million Americans lack basic skills needed to access, understand, and use health information and services to make healthy dietary choices. Effective teaching by physicians can bridge the learning gap and arrest the epidemic of obesity. The Academy at Harvard Medical School is developing best practices in teaching that will equip future doctors to reduce health illiteracy and promote positive changes in thinking and behavior in their patients. Models of how people learn can help physicians select tasks, questions, and prompts that advance teaching and learning. To keep and use new information, adults need to integrate new ideas into existing frameworks of understanding and participate in the learning process by linking new information to what is already known. By teaching patients how to read a single food label, starting with calories, physicians can set the stage for future learning. The process of change is challenging, particularly in adults. Best practices in teaching and learning can help physicians be more effective agents of change.
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PMID:Teaching, learning, doing: best practices in education. 1600 24

Although obesity is associated with increased risk of many chronic diseases including cardiovascular disease, diabetes, hypertension, and cancer, there is little evidence to suggest that obesity increases risk of osteoporosis. In fact, both weight and body mass index (BMI) are positive predictors of bone mass in adults, suggesting that those who are overweight or obese may be at lower risk of osteoporosis. However, recent evidence suggests that in children and adolescents, obesity may be associated with lower rather than higher bone mass. To understand the relation of fat mass to bone mass, we examined data gathered from an ethnically diverse group of 921 young women, aged 20-25 years (317 African Americans, 154 Asians, 322 Caucasians, and 128 Latinas) to determine how fat mass (FM) as well as lean tissue mass (LTM) is associated with bone mass. Bone mass, FM, and LTM were measured using dual energy X-ray absorptiometry (GE Lunar Corp, Madison, WI). Bone mass was expressed as bone mineral density (BMD; g/cm2) and bone mineral apparent density (BMAD; g/cm3) for the spine and femoral neck, and as BMD and bone mineral content (BMC; g) for the whole body. Regression techniques were used to examine the following: (1) in separate equations, the associations of LTM and FM with each bone mass parameter; and (2) in the same equation, the independent contributions of LTM and FM to bone mass. LTM and FM were positively correlated with BMD at all skeletal sites. When the contributions of FM and LTM were examined simultaneously, both FM and LTM continued to be positively associated with bone mass parameters but the effect of FM was noted to be smaller than that of LTM. We conclude that in young women, LTM has a greater effect than fat mass on bone density per kg of tissue mass.
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PMID:The relative contributions of lean tissue mass and fat mass to bone density in young women. 1604 Feb 85

Obesity is now the most common disorder of childhood in the developed world, and its prevalence is still increasing. A large body of high-quality and consistent evidence shows that it is best defined using the body mass index (BMI) percentile relative to national BMI reference data. This definition diagnoses excessive fatness adequately, and denotes increased risk of adverse health outcomes. Future research may provide improved obesity definitions for epidemiological use, so that the obesity epidemic can be monitored more effectively. Paediatric obesity causes ill health in both childhood and adulthood, though further research is required on the economic consequences, on some of the co-morbidities in childhood (notably psychological morbidity), and in adulthood where the amount of empirical evidence on long-term effects is limited. The combination of high prevalence with adverse consequences has created a public health crisis.
Best Pract Res Clin Endocrinol Metab 2005 Sep
PMID:Descriptive epidemiology and health consequences of childhood obesity. 1615 Mar 78

Obesity in children arises from a complex interplay between genetic susceptibility and behaviour, primarily relating to dietary habits and physical activity. Evidence for specific behavioural factors that promote or protect against excess weight gain in children is more limited than in adults, and the effects of growth and development are not clear. A number of behavioural risk factors has been postulated, including diets with a high energy density, high consumption of sugar-sweetened beverages, large portion sizes, eating patterns, high levels of sedentary behaviour and low levels of physical activity. However, most evidence is derived from cross-sectional studies which frequently yield conflicting results. More prospective studies with accurate measures of exposures and outcomes in terms of body composition are needed to provide more robust evidence on which to base interventions to achieve long-term behavioural change and prevent excess weight gains in children.
Best Pract Res Clin Endocrinol Metab 2005 Sep
PMID:Behavioural determinants of obesity. 1615 Mar 79

Genetic factors are involved in the regulation of body weight and in determining individual responses to environmental factors such as diet and exercise. The identification and characterization of monogenic obesity syndromes have led to an improved understanding of the precise nature of the inherited component of severe obesity and has had undoubted medical benefits, whilst helping to dispel the notion that obesity represents an individual defect in behaviour with no biological basis. For individuals at highest risk of the complications of severe obesity, such findings provide a starting point for providing more rational mechanism-based therapies, as has successfully been achieved for one disorder, congenital leptin deficiency.
Best Pract Res Clin Endocrinol Metab 2005 Sep
PMID:Genetic and hereditary aspects of childhood obesity. 1615 Mar 80

Nutrition is an important regulator of the tempo of human growth. Infancy may represent a critical "window" where variations in nutrition have longer-term consequences for growth and development. Rapid weight gain during infancy is associated with accelerated growth and early pubertal development. Rapid weight gain in infancy is also associated with the development of insulin resistance and an exaggerated adrenarche. Such circulating hormonal changes, together with elevated leptin levels and integral effects of fat cells on hormone action through local 11beta-steroid dehydrogenase and aromatase activity could effect rate of progression of pubertal development in obese subjects. The secular trends in growth and maturation are partly attributed to changing nutrition. Recent data suggest that age at menarche may be static, but there is a debate as to whether the first signs of puberty are being seen much earlier in obese girls. Rapid early weight gain, obesity and early development may have implications for later health through the development of PCOS and overall association with cancer risk.
Best Pract Res Clin Endocrinol Metab 2005 Sep
PMID:Effects of obesity on growth and puberty. 1615 Mar 81

The present article addresses the hypothesis that inefficient skeletal muscle lipid utilization may relate to the development of obesity and insulin resistance. In practice, there is evidence of impaired muscle fatty acid utilization in the obese state, and studies indicate that differences in muscle fatty acid oxidative capacity might play a role in the pathogenesis of obesity. The link between obesity and insulin resistance has been recognized for many years. There is accumulating evidence that a disturbed muscle fat oxidative capacity results in the accumulation of the lipid intermediates diacylglycerol and Fatty acid acyl coenzyme A (CoA), which may interfere with insulin signaling and result in an inhibition of insulin-mediated glucose uptake. Underlying mechanisms for disturbed fatty acid handling may relate to impaired adipose tissue lipolysis, abnormal muscle fatty acid uptake and a reduced ability to oxidize fat. Many of these abnormalities have been reported both in the obese and the type 2 diabetic state. The role of obesity per se in these disturbances is an important question that needs to be addressed.
Best Pract Res Clin Endocrinol Metab 2005 Sep
PMID:Metabolic fluxes in skeletal muscle in relation to obesity and insulin resistance. 1615 Mar 82

The prevalence of childhood obesity is increasing worldwide, as is the prevalence of obesity-related co-morbidity. Altered glucose metabolism, manifested as impaired glucose tolerance (IGT), appears early in obese children and adolescents. Obese young people with IGT are characterized by marked peripheral insulin resistance and a relative beta-cell failure. Lipid deposition in muscle and the visceral compartment, and not only adiposity per se, is related to increased peripheral insulin resistance, the "driving force" of the metabolic syndrome. Other elements of the metabolic syndrome, such as dyslipidemia and hypertension, are already present in obese youngsters and worsen with the degree of obesity. Similarly, markers of systemic "low-grade inflammation" worsen with increasing adiposity. The long-term impact on cardiovascular and liver morbidity of obesity-related insulin resistance in young people is expected to emerge as these youngsters become young adults.
Best Pract Res Clin Endocrinol Metab 2005 Sep
PMID:The metabolic consequences of childhood obesity. 1615 Mar 83


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