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

A public health strategy carries more constraints than a high risk strategy because it targets both low risk and high risk individuals; this requires cautious intervention and hence achieves only a modest reduction in risk. Nevertheless, a modest population-wide fall in the concentrations of atherogenic lipoproteins leads to substantial numbers of preventable heart attacks and deaths. Other strategic considerations are to lower non-lipid cardiovascular risks (hypertension, clotting tendency) and to prevent other diet-related disease (such as cancer) through interventions which lower plasma lipids. The major nutritional changes which achieve this are optimising energy balance, reducing total fats and saturated fatty acids and increasing plant foods which are rich sources of unsaturated fatty acids, fibre and antioxidants. Each of these contributes to optimising the low density lipoprotein (LDL) concentration. Antioxidants (vitamins C and E mainly) may inhibit LDL oxidation. The strategy for lowering plasma triglyceride, especially in the context of atherogenic lipoprotein phenotypes, is mainly through energy balance, reduced saturated fat and alcohol. Correcting overweight especially in those with abdominal obesity, may normalise raised plasma triglyceride, low high density lipoprotein (HDL), abnormal LDL and even glucose intolerance and hypertension, which may be associated. The scientific basis for the lipid optimising effects of the different nutrients will be discussed.
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PMID:Optimising plasma lipids: public intervention versus high risk management. 144 40

All large prospective studies (n greater than 20,000) and several smaller studies have found that severe obesity [body mass index (BMI) greater than or equal to 35 kg/m2] is associated with approximately a twofold increase in total mortality and in a severalfold increase in mortality due to diabetes, cerebro-, and cardiovascular disease, and certain forms of cancer. Studies that have not been able to confirm this have been small and/or short term, have failed to control for smoking or early mortality, have controlled for intermediate risk factors in an inappropriate way, or have a reduced internal validity due to misclassification biases. As compared with BMI, abdominal obesity is a stronger predictor of mortality in most studies available. The incidence of sudden death unexplained by autopsy may be up to 40 times higher in severely obese subjects as compared with the general population. A small weight increase since the age of 18 is associated with a decreased risk whereas weight increases greater than 10 kg are associated with an increased mortality. The total mortality ratio for severe obesity decreases from 55 y of age and is not detectable above 80 y of age. Studies lacking adequate control groups indicate that a sustained weight loss may induce a reduced mortality but results from controlled intervention studies are so far not available.
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PMID:Mortality of severely obese subjects. 153 Oct 97

Whereas up to the end of the last century overweight reflected the privilege of the high society and her relative good health, the recent epidemiological studies have assessed the relations between body weight and general or cause specific morbidity and mortality. The major diseases associated with obesity are hypertension, atherosclerosis and diabetes, as well as certain types of cancer. Less well known complications include hepatic steatosis, gallbladder diseases, pulmonary function impairment, endocrine abnormalities, obstetric complications, trauma to the weight bearing joints, gout, cutaneous diseases, proteinuria, increased hemoglobin concentration and possibly immunologic impairments. From these wide epidemiological studies arise the definition of obesity: with an excess of 20% beyond the desirable weight, the complications bound to the overweight become statistically more frequent. Over there a U or J shaped curve illustrates the relation between the overweight and the degree of these various complications. An excess of 45 kg or more represents the critical level which defined "morbid obesity" with its own complications, the most important are sudden unexplained death, ventilatory disorders, circulatory congestion and functional limitations in activities of daily living and of course psychological consequences. When for certain complications, such as diabetes, the relationship with the overweight is evident, discrepancies between certain studies, especially for the cardiovascular diseases, had focused the attention on the regional patterns of fat distribution. Cross-sectional studies have shown abdominal obesity to be strongly associated with risk factors for cardiovascular disease, stroke and death independent of the total degree of obesity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The contribution of epidemiology to the definition of obesity and its risk factors]. 266 68

Abdominal obesity increases the estrogen-to-androgen ratio and may increase sympathetic nervous activity, both hypothesized to influence the development of benign prostatic hyperplasia and the severity of urinary obstructive symptoms. In 1986 and 1987, men aged 40-75 years who were participants in the Health Professionals Follow-up Study and who were without prior diagnosis of cancer or prostatectomy provided data on weight, height, and waist and hip circumferences. The men were followed for incidence of prostatectomy for benign prostatic hyperplasia up to January 1992. In addition, the frequency and severity of symptoms of urinary obstruction were assessed among respondents to a questionnaire in 1992. Among 25,892 men who provided complete information for both surgery and symptoms, 837 men had surgery for benign prostatic hyperplasia, and 2,581 of those without surgery reported frequent urinary symptoms. After adjustment for age, smoking, and body mass index, abdominal obesity was related to prostatectomy (odds ratio (OR) = 2.38, 95% confidence interval (CI) 1.42-3.99, for those with a waist circumference > or = 43 inches (109 cm) relative to those with a waist circumference < 35 inches (89 cm); p trend < 0.0001) and with frequent urinary symptoms among those without prostatectomy (OR = 2.00, 95% CI 1.47-2.72; p < 0.0001). Body mass index, hip circumference, and waist-to-hip ratio were not associated with benign prostatic hyperplasia independently of waist circumference. These results suggest that abdominal obesity in men may increase the frequency and severity of urinary obstructive symptoms and may increase the likelihood that such obese men will undergo a prostatectomy.
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PMID:Obesity and benign prostatic hyperplasia. 752 82

Two long and broad streams of medical literature, from the 1950's to date, have established the existence of two unrelated abnormalities of androgen production in women with breast cancer. One is the genetically determined presence of subnormal production of adrenal androgens (i.e. DHEA and DHEAS) in women with premenopausal breast cancer and their sisters, who are at increased risk for breast cancer. The other is excessive production of testosterone, of ovarian origin, in subsets of women with either premenopausal or postmenopausal breast cancer and women with atypical breast-duct hyperplasia, who are at increased risk for breast cancer; along with the hypertestosteronism, there is frequently chronic anovulation in the premenopausal patients. The combination of ovarian hypertestosteronism and chronic anovulation is characteristic of the polycystic ovary syndrome and is also frequently seen in women with abdominal ("android") obesity; both PCOS and abdominal obesity are known to be characterized by high risk for postmenopausal cancer. The elevated testosterone levels and the increased levels of insulin, IGF-I, and IGF-II that are seen in PCOS and abdominal obesity could favor the development of breast cancer in several ways, all of which have been demonstrated experimentally: binding of testosterone to cancer cells bearing testosterone receptors, with direct stimulation; intratissular aromatization of testosterone to estradiol, with stimulation of estrogen-sensitive cells; stimulation of the production of epithelial growth factor (EGF) by testosterone, with direct mitogenic effect of EGF on cancer cells; stimulation of aromatase by insulin and IGF-I; direct mitogenic stimulation of cancer cells by insulin, IGF-I, and IGF-II; and stimulation by IGF-I and IGF-II of the intratissular reduction of estrone to estradiol. Since PCOS is probably largely genetically determined, and abdominal obesity may also be, the hypertestosteronism of these conditions may represent a second genetically determined hormonal risk factor for breast cancer.
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PMID:Abnormal production of androgens in women with breast cancer. 784 May 9

It is postulated that the metabolic/endocrine concomitants of insulin resistance resulting from high animal fat intake and weight gain after the age of 30 could be contributing to the increasing incidence of postmenopausal breast cancer and recent changes in its biologic characteristics. Case/control studies have shown that hyperinsulinaemia and abdominal obesity, which are recognized as markers of insulin resistance, are risk markers for postmenopausal breast cancer also. Excess weight gain linked to high dietary intake of saturated fat is thought to be a major cause of insulin resistance. The hypothesis is compatible with the "breast tissue age" model for breast cancer risk. Biological evidence suggests that the concomitants of insulin resistance may stimulate growth activity in existing breast cancer also. The hypothesis that nutritional factors which favour hyperinsulinaemia may also favour breast cancer growth can be tested. Restriction of dietary fat and high intake of fibre and complex carbohydrate have been shown to normalise insulin levels in a proportion of subjects with hyperinsulinaemia. Restriction of dietary fat intake has also been shown to reduce bioavailable oestrogen levels in healthy postmenopausal women. A randomised trial of a low fat, high fibre, high complex carbohydrate regimen is proposed as adjuvant treatment following primary surgery in postmenopausal women with early breast cancer. A cancer preventive or delaying ability can be assessed by comparing the incidence of contralateral second breast cancer and the metastasis rate in the diet and control groups. Insulin levels, abdominal obesity, and body mass should be monitored although normalisation of insulin levels need not necessarily involve decrease in body mass.
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PMID:Nutrition and breast cancer risk: can an effect via insulin resistance be demonstrated? 873 75

Individuals whose energy intake exceeds expenditure are at increased risk of colorectal cancer. To determine whether body-size measurements at different ages were risk factors for cancer of the colon-rectum, we carried out a hospital-based case-control study in 6 Italian areas, 2 of which were in the South. Interviews were conducted with 1,217 subjects of both genders with incident histologically confirmed cancer of the colon, 726 with cancer of the rectum, and 4,136 controls hospitalized for acute, non-neoplastic, non-digestive conditions. The questionnaire included information on sociodemographic factors, and physical activity, a validated dietary history, height, weight at diagnosis and at 12, 30 and 50 years of age and waist-to-hip ratio (WHR). After allowance for education, physical activity, energy intake, family history of colorectal cancer and recent change in weight, the body-mass index (BMI) was significantly associated with colorectal-cancer-risk in men (odds ratio, OR, in highest vs. lowest quintile = 1.7; 95% confidence interval, CI, 1.3-2.3), but not in women (corresponding OR = 0.9; 95% CI, 0.7-1.2). Cases of both gender tended to have higher BMI than controls in adolescence, young adulthood and middle age. Height appeared unrelated to risk. In women, but not in men, WHR was positively associated with risk, independently of BMI (OR for > or = 0.90 vs. < or = 0.81 = 1.6; 95% CI; 1.2-2.1). Thus, excessive weight predicts colorectal-cancer risk in men, whereas abdominal obesity (i.e., a high WHR) represents a more reliable risk indicator in women.
Int J Cancer 1998 Oct 05
PMID:Body size and colorectal-cancer risk. 975 46

This review examines evidence that weight gain in the years leading up to the menopause can contribute to a woman's risk of postmenopausal breast cancer and may involve perimenopausal stimulation of growth in cancer precursor lesions. We used the Medline database since 1980 to examine studies that assessed the association between increased risk of postmenopausal breast cancer and perimenopausal weight gain or abdominal fat accumulation. This review examines possible mechanisms by which the endocrine-metabolic concomitants of hyperinsulinemia may act as late-stage promoters of mammary carcinogenesis. It was found that, in obese postmenopausal women with breast cancer, excess weight is likely to have been gained before menopause. In Western women, evidence of abdominal obesity associated with hyperinsulinemia increases progressively after the age of 40. Weight gain in the years leading up to the menopause mainly involves abdominal obesity which is associated with insulin resistance, increased free estrogen levels, and imbalance in sex steroids levels. These endocrine-metabolic changes are likely to inhibit the tendency for cancer precursor lesions to regress at the menopause and may lead to late-stage promotion of mammary carcinogenesis.
Cancer Detect Prev 1999
PMID:Perimenopausal weight gain and progression of breast cancer precursors. 989 88

Obesity has been related to increased risk of colon cancer or adenomas, but the epidemiologic findings are not entirely consistent. We examined the relation of not only body mass index (BMI) but also waist-to-hip ratio (WHR) and weight gain to colon adenoma risk in men who received a preretirement health examination at the Japan Self Defense Forces (SDF) Fukuoka and Kumamoto Hospitals during the period from 1995 to 1996. In the series of 803 men at age 47-55 years, 189 cases of colon adenomas and 226 controls with normal total colonoscopy were identified. Weight at 10 years before was ascertained by referring to the recorded data. After allowance for hospital, rank in the SDF, smoking and alcohol use, weight gain over the past 10 years was significantly associated with increased risk of colon adenomas (odds ratio for > or = 6 kg versus < or =-2 kg = 2.2; 95% confidence interval 1.0-4.8). High BMI and high WHR were each associated with increased risk, but only WHR was related to the risk independently of weight gain. In particular, weight gain accompanied with a high WHR was associated with a significant increase in the risk. Men with high physical activity tended to have lower risk. Associations with obesity-related variables and physical activity were not materially differential as regards the location and size of adenoma. The findings indicate that weight gain in middle age leading to abdominal obesity increases the risk of colon adenomas, and consequently of colon cancer.
Jpn J Cancer Res 1999 Aug
PMID:Obesity, weight gain and risk of colon adenomas in Japanese men. 1054 50

Epidemiological studies on risk factors for CRC have focused mainly on diet. In any case, the results of these studies show several inconsistencies, except for the beneficial role of high intake of vegetables and, to some lesser extent, of fruit. Weight and height have also been studied, partly because they reflect the balance between energy intake and expenditure in different age periods. Energy intake, body size and physical activity will be reviewed in this paper focusing mostly on recent data coming from Italian, English and Scandinavian studies. Overweight has long been recognized as a risk factor for hormone related and other cancers and this is confirmed not simply from case-control studies but from large cohort studies as well. The major findings of recent Italian studies are that excessive weight at various ages predicts colorectal cancer risk in men while in women, abdominal obesity, as indicated by a high WHR, represents a more reliable risk indicator. If all men could reduce their BMI below 25, about 9% of male colorectal cancer might be avoided in Italy. A decrease of WHR below 0.82 might reduce colorectal cancer in women by 19%. In addition, the epidemiological evidence consistently shows that physical activity reduces the risk of colon cancer. On the contrary, evidence on rectal cancer is less impressive. Some uncertainty still exists in relation to the intensity and duration of physical activity. In conclusion, body size control along all life and physical activity represent important factors to prevent colon cancer and a wide range of chronic conditions. Therefore, strategies to favour these goals through counselling from health-care providers, regulatory changes and programs aimed at individuals and communities should be implemented.
Eur J Cancer Prev 1999 Dec
PMID:Energy intake, overweight, physical exercise and colorectal cancer risk. 1077 19


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