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Query: UMLS:C0311277 (abdominal obesity)
 2,792 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Obesity and overweight, as a part of the metabolic syndrome, are well known risk factors for the development of diabetes, hypertension, coronary heart disease, hyperlipidemia, stroke, sleep apnea syndrome, osteoarthritis and certain forms of cancer. Cardiovascular disease remains the leading killer in industrialized countries, where it accounts for 40% of deaths. Obesity is defined either by increased waist circumference, waist to hip ratio, or body mass index. Obesity results from an interaction of genes and lifestyle. As people in both developed and developing countries eat more and more energy dense food, and have ever less physical activity, the number of overweight and obese people increases to epidemic proportions. Abdominal obesity plays a key role in the pathophysiology of metabolic disorders, is associated with insulin resistance, and predicts the development of type 2 diabetes and subsequent coronary artery disease. In the general population, obesity is associated with an increased mortality, but paradoxically, a positive correlation between body mass index and survival in congestive heart failure has been reported. In secondary prevention, obesity is underrecognized, underdiagnosed and undertreated in persons with cardiovascular diseases. Weight loss and prevention of weight gain have to be considered one of the most important strategies to reduce the incidence of cardiovascular disease. Increased physical activity and appropriate diet are the cornestones of treatment. Considering the high prevalence of overweight and obesity in Croatia, there is urgent necessity to improve the level of knowledge and skills in understanding obesity by health care services, and to implement appropriate professional strategy to achieve the desired lifestyle modifications.
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PMID:[Obesity--a global public health problem]. 1758 71

Although obesity is an established risk factor for renal cell carcinoma, the possible effect of central adiposity and long-term variation in weight has yet to be established. The authors studied 140,057 women aged 50-79 years enrolled in the Women's Health Initiative in the United States to examine the role of obesity, especially abdominal obesity, and weight cycling in relation to risk of renal cell carcinoma among postmenopausal women. Cox models were used to estimate relative risks and their corresponding 95% confidence intervals. During an average of 7.7 years of follow-up through September 12, 2005, a total of 269 incident cases of renal cell carcinoma were identified. Central adiposity, as indicated by waist-to-hip ratio, was an important risk factor for developing renal cell carcinoma (highest vs. lowest quartile: relative risk = 1.8, 95% confidence interval: 1.2, 2.5; p for trend = 0.0003). Moreover, women who had experienced weight cycling more than 10 times were at 2.6 times (95% confidence interval: 1.6, 4.2) increased risk compared with women whose weight was stable. Results add evidence that obesity, particularly central adiposity, is associated with an increased risk of renal cell carcinoma among postmenopausal women. Furthermore, they indicate that weight cycling is independently associated with further increased risk of this malignancy.
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PMID:Body size, weight cycling, and risk of renal cell carcinoma among postmenopausal women: the Women's Health Initiative (United States). 1834 11

Although obesity has been consistently linked to an increased risk of several malignancies, including cancers of the colon, gallbladder, kidney, and pancreas, its role in prostate cancer etiology remains elusive. Data on the association between obesity and prostate cancer incidence are inconsistent, and in some studies obesity is associated with an increase in risk of high-grade prostate cancer but with a decrease in risk of low-grade tumors. In contrast, obesity has been consistently associated with an increased risk of prostate cancer aggressiveness and mortality. The differential effects of obesity on subtypes of prostate cancer suggest etiologic heterogeneity in these tumors and complex interactions between androgen metabolism and several putative risk factors, including insulin resistance, diabetes, inflammation, and genetic susceptibility, on prostate cancer risk. Data on the role of abdominal obesity, insulin resistance, and metabolic syndrome in prostate cancer etiology are limited. Obesity has been shown to be associated with a state of low-grade chronic inflammation, and insulin resistance and the metabolic syndrome are associated with adverse metabolic profiles and with higher circulating concentrations of inflammation-related markers, including leptin, interleukin-6, and tumor necrosis factor-, many of which have been shown to enhance tumor growth. Thus, whether obesity and metabolic syndrome modulate the risk of prostate cancer through chronic inflammation needs to be investigated further. Given that the prevalence of obesity and metabolic syndrome is increasing worldwide and that the world population is aging, the roles of obesity and metabolic syndrome in prostate carcinogenesis warrant further clarification.
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PMID:Obesity, metabolic syndrome, and prostate cancer. 1826 78

Calorie intake is an important determinant of health. Excessive energy intake is associated with abdominal obesity, type 2 diabetes, cardiovascular disease, cancer, and premature mortality. Calorie restriction (CR) without malnutrition increases maximal lifespan by preventing many age-associated chronic diseases and by preserving function at more youthful-like states in rodents. In overweight and obese humans CR improves metabolic health and reduced mortality for type 2 diabetes, cardiovascular disease and cancer. In middle-aged healthy lean individuals CR causes many of the same cardiometabolic adaptations that occur in long-lived CR rodents, including decreased metabolic, inflammatory, and hormonal risk factors for diabetes, hypertension, cardiovascular disease and cancer Protein and polyphenols intake, and physical activity may have additional beneficial effects in preventing diseases and promoting health. Additional studies are needed to identify the precise calorie, protein and polyphenols intake and amount of exercise needed for optimal health in each individual, depending on his/her age, sex and genetic background.
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PMID:[Nutrition, adiposity and health]. 1827 33

An epidemic of overweight/obesity and type 2 diabetes, caused by overeating nutrient-poor energy-dense foods and a sedentary lifestyle, is spreading rapidly throughout the world. Abdominal obesity represents a serious threat to health because it increases the risk of developing many chronic diseases, including cardiovascular disease and cancer. Calorie restriction (CR) with adequate nutrition improves cardiometabolic health, prevents tumorigenesis and increases life span in experimental animals. The purpose of this review is to evaluate the metabolic and clinical implications of CR with adequate nutrition in humans, within the context of data obtained in animal models. It is unlikely that information regarding the effect of CR on maximal life span in humans will become available in the foreseeable future. In young and middle-aged healthy individuals, however, CR causes many of the same cardiometabolic adaptations that occur in long-lived CR rodents, including decreased metabolic, hormonal and inflammatory risk factors for diabetes, hypertension, cardiovascular disease and cancer. Unraveling the mechanisms that link calorie intake and body composition with metabolism and aging will be a major step in understanding the age-dependency of a wide range of human diseases and will also contribute to improve the general quality of life at old ages.
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PMID:Calorie restriction and cardiometabolic health. 1827 79

Obesity has become epidemic in the United States, in Europe, and in many urban areas in the developing world. The globalization of certain 'fast foods' and 'soft drinks' may, in part, be contributing to this epidemic. Diets high in saturated fatty acids and trans fats as well as drinks that have high fructose corn syrup levels may be particularly harmful. Recent research suggests that fat is a dynamic endocrine organ and that visceral fat is associated with the metabolic syndrome. Central obesity leads to organ steatosis and altered serum adipokines including reduced adiponectin and markedly elevated leptin. This abnormal adipokine milieu results in increased tissue infiltration of monocytes and macrophages which produce proinflammatory cytokines that alter organ function. Over many years, the combination of steatosis and local inflammation leads to fibrosis and eventually to cancer. Nonalcoholic fatty liver disease (NAFLD) is a precursor for nonalcoholic steatohepatitis (NASH). NAFLD and NASH (1) lead to cirrhosis and hepatocellular carcinoma, (2) increase the risk of liver resection, and (3) compromise the outcome of liver transplantation. Similarly, in the pancreas nonalcoholic fatty pancreas disease (NAFPD) may lead to nonalcoholic steatopancreatitis (NASP). NAFPD and NASP may (1) promote the development of chronic pancreatitis and pancreatic cancer, (2) exacerbate the severity of acute pancreatitis, and (3) increase the risk of pancreatic surgery. In the gallbladder nonalcoholic fatty gallbladder disease (NAFGBD, cholecystosteatosis) may lead to steatocholecystitis. Cholecystosteatosis may be an explanation for (1) the increased incidence of chronic acalculous cholecystitis and (2) the increased number of cholecystectomies.
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PMID:Hepato-pancreato-biliary fat: the good, the bad and the ugly. 1833 22

Adiponectin is an adipocyte-derived protein with an insulin-sensitizing action. Circulating levels of adiponectin are inversely correlated with obesity, especially abdominal obesity. Some studies have suggested that low levels of circulating adiponectin might be related to increased risk of colorectal cancer and adenomas. The present study examined the relationship between total and high-molecular-weight (HMW) adiponectin to colorectal adenomas in the Self Defense Forces (SDF) Health Study. The study subjects comprised 656 cases of colorectal adenomas and 648 controls with normal colonoscopy among men receiving a preretirement health examination at two Self Defense Forces hospitals. Total and HMW adiponectin were slightly lower in adenoma cases than in controls; geometric means of total adiponectin were 5.42 microg/mL in cases and 5.63 microg/mL in controls (P = 0.13), and the corresponding values of HMW adiponectin were 2.47 microg/mL and 2.57 microg/mL, respectively (P = 0.29). Regardless of adjustment for body mass index and other lifestyle factors, total adiponectin was unrelated to the risk of colorectal adenomas. Total adiponectin levels were inversely related to the risk of large adenomas (>or= 5 mm), but not of small adenomas, with a nearly statistically significant decreasing trend (P = 0.06). However, the inverse association was largely ascribed to body mass index and other lifestyle factors. HMW adiponectin showed no clear association with either overall or size-specific risk of colorectal adenomas. The study provided suggestive evidence for a protective association between adiponectin and large adenomas, but did not indicate a protective association independent of adiposity.
Cancer Sci 2008 Apr
PMID:Adiponectin and colorectal adenomas: Self Defense Forces Health Study. 1837 27

Risk factors are generally shared between men and women with the major differences being hormonal. Nine modifiable risk factors account for over 90% of the risk of a coronary event in men and women--smoking, hypertension, hyperlipidaemia, diabetes, abdominal obesity, lack of exercise, alcohol excess, reduced intake of fruit and vegetables, and psychosocial issues. Approximately half the decline in deaths from coronary heart disease (CHD), between 1980 and 2000, can be attributed to a reduction in the major risk factors and the other half to the use of evidence-based management. As educational efforts to increase awareness of cardiovascular disease (not cancer) to be the leading cause of death and disability in women are also associated with preventative action, it is important that health-care professionals educate themselves about CHD in women and communicate with women themselves, so that women can come forward for advice and evaluation.
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PMID:Gender differences in cardiovascular disease prevention. 1838 Sep 55

The prevalence of obesity, defined as a BMI of > or =30.0 kg/m2, has increased substantially over previous decades to about 20% in industrialized countries, and a further increase is expected in the future. Epidemiological studies have shown that obesity is a risk factor for: post-menopausal breast cancer; cancers of the endometrium, colon and kidney; malignant adenomas of the oesophagus. Obese subjects have an approximately 1.5-3.5-fold increased risk of developing these cancers compared with normal-weight subjects, and it has been estimated that between 15 and 45% of these cancers can be attributed to overweight (BMI 25.0-29.9 kg/m2) and obesity in Europe. More recent studies suggest that obesity may also increase the risk of other types of cancer, including pancreatic, hepatic and gallbladder cancer. The underlying mechanisms for the increased cancer risk as a result of obesity are unclear and may vary by cancer site and also depend on the distribution of body fat. Thus, abdominal obesity as defined by waist circumference or waist:hip ratio has been shown to be more strongly related to certain cancer types than obesity as defined by BMI. Possible mechanisms that relate obesity to cancer risk include insulin resistance and resultant chronic hyperinsulinaemia, increased production of insulin-like growth factors or increased bioavailability of steroid hormones. Recent research also suggests that adipose tissue-derived hormones and cytokines (adipokines), such as leptin, adiponectin and inflammatory markers, may reflect mechanisms linked to tumourigenesis.
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PMID:Obesity and cancer. 1841 87

Though obesity is an established risk factor for gall bladder cancer, its role in cancers of the extrahepatic bile ducts and ampulla of Vater is less clear, as also is the role of abdominal obesity. In a population-based case-control study of biliary tract cancer in Shanghai, China, odds ratios (ORs) and 95% confidence intervals (CIs) were calculated for biliary tract cancer in relation to anthropometric measures, including body mass index (BMI) at various ages and waist-to-hip ratio (WHR), adjusting for age, sex, and education. The study included 627 patients with biliary tract cancer (368 gall bladder, 191 bile duct, 68 ampulla of Vater) and 959 healthy subjects randomly selected from the population. A higher BMI at all ages, including early adulthood (ages 20-29 years), and a greater WHR were associated with an increased risk of gall bladder cancer. A high usual adult BMI (>or=25) was associated with a 1.6-fold risk of gall bladder cancer (95% CI 1.2-2.1, P for trend <0.001). Among subjects without gallstones, BMI was also positively associated with gall bladder cancer risk. Regardless of BMI levels, increasing WHR was associated with an excess risk of gall bladder cancer risk, with those having a high BMI (>or=25) and a high WHR (>0.90) having the highest risk of gall bladder cancer (OR=12.6, 95% CI 4.8-33.2), relative to those with a low BMI and WHR. We found no clear risk patterns for cancers of the bile duct and ampulla of Vater. These results suggest that both overall and abdominal obesity, including obesity in early adulthood, are associated with an increased risk of gall bladder cancer. The increasing prevalence of obesity and cholesterol stones in Shanghai seems at least partly responsible for the rising incidence of gall bladder cancer in Shanghai.
Br J Cancer 2008 Sep 02
PMID:Body size and the risk of biliary tract cancer: a population-based study in China. 1872 71


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