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

In postmenopausal women estrogens alone are effective in reversing vasomotor symptoms and vaginal atrophy. They also prevent the bone loss associated with osteoporosis and reduce the risk of cardiovascular disease, probably through their beneficial effects on lipid metabolism. Unopposed long-term estrogen therapy, however, increases the risk of developing endometrial hyperplasia, endometrial cancer, and possibly breast cancer as well. The risk of developing endometrial cancer can be reduced by combining a progestin with the estrogen, by controlling obesity, and by rigorous clinical screening and surveillance. The effect of progestins on the risk of developing breast cancer is still controversial. Although some progestins may reverse the cardioprotective effect of estrogens, those with minimal androgenicity appear less likely to do so. Hormone replacement therapy that combines estrogen with a progestin of minimal androgenicity is thus a rational alternative to unopposed estrogen therapy. Current epidemiologic knowledge suggests that the benefits of hormone replacement therapy, with or without any progestins, strongly outweigh the risks.
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PMID:The benefits and risks of hormone replacement therapy: an epidemiologic overview. 160 89

In a case-control study involving 268 cases of endometrial cancer and an equal number of population controls, we assessed the relationship of risk to body weight and fat distribution, examining weight at various ages and current anthropometric measurements. Weight gain during later adulthood and resultant high body masses were important risk predictors, indicating that obesity is an important risk factor, even in an area where the prevalence of obesity and incidence of endometrial cancer are low. Certain fat distribution patterns were related to risk of endometrial cancer independent of general obesity. In particular, fat deposits on the trunk were associated with elevated risks, with the odds ratio for the highest versus lowest quartile of subscapular skinfolds remaining significant even after adjustment for body mass index (odds ratio = 2.9; 95% confidence interval, 1.1-7.3). Central versus peripheral obesity, as measured by the subscapular:triceps ratio, also was related to increased risk, although the association failed to remain significant after adjustment for body mass (highest to lowest quartile, odds ratio = 1.7). In contrast, upper body obesity, as assessed by the waist:thigh ratio, was unrelated to risk. These results support the need for future studies assessing the relationship of hormonal and other biological parameters of fat distribution to assist in identifying causal mechanisms for this tumor.
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PMID:Relation of obesity and body fat distribution to endometrial cancer in Shanghai, China. 161 61

Obesity is associated with many comorbid disease states including neoplasia. The increased risk of developing endometrial cancer is thought to be due to the higher level of circulating estrogens in obese women. Uterine leiomyomata (fibroids) are also thought to be influenced by estrogens. To determine whether patients presenting with symptomatic uterine fibroids were more obese than the general population, we retrospectively reviewed the hospital records of 144 women who underwent either hysterectomy or myomectomy for uterine fibroids. Obesity was defined as preoperative weight greater than 120% of desirable body weight (DBW) for the patient's height. In our investigation, 51% of the study population were obese. Moreover, 16% were severely obese (defined as greater than 150% DBW). When compared with the general population of women in the United States matched for height and age, the study population was significantly heavier. (p less than 0.0002). Patient age, parity, menopausal status, and degree of obesity did not correlate with the number of fibroids within the uterus. Fibroid size was significantly larger in nulliparous women (p less than 0.005). These results suggest that symptomatic uterine fibroids may be another comorbid disease state associated with obesity.
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PMID:Relationship between obesity and uterine leiomyomata. 180 14

Precanceroses and early screening of endometrial carcinomas are reviewed. Measures are evaluated on how to prevent this malignancy with administration of gestagens in hyperplastical endometrial changes in climacteric conditions and manifestations of endometrial estrogenization in postmenopause. On the basis of clinical, laboratory and histological investigations, the total of 31 female subjects with dysfunctional bleeding was given medroxyprogesterone acetate (Provera Upjohn tbl.) in 10 mg daily doses for up to 10-13 days cyclically prior to the onset of menopause. Under the mentioned treatment any of them experienced the rebleed, and no endometrial carcinoma had been diagnosed with control vacuum curettage within one year of observation. In a total of 196 women operated on to endometrial carcinoma, the occurrence of risk-factors for the development of mentioned tumour (obesity, late menopause, i.e. menopause after 50 years of age, sterility and dysfunctional bleeding backed with anovulation, long-term estrogen administration, feminizing ovarian tumours, liver diseases, glycide metabolic disorders and hypertension) was evaluated. The present work was aimed on the screening of asymptomatic group of women. Two important signs (obesity and late menopause) were invariably determined with the addition of any other risk factor. Mentioned women are supposed to undergo regular yearly histological investigation of endometrium. Of most benefit the vacuum curettage is believed by authors as a result of comparing the validation of cytological and histological methods in order of early evidence.
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PMID:[Precanceroses and endometrial carcinoma]. 184 15

To further characterize the association of obesity and endometrial cancer, in particular with regard to the role of early-age obesity and adult weight gain, the authors assembled by computer linkage a population-based historical cohort of 30,266 women born between 1913 and 1932, for whom weight and height had been recorded in 1942-43 and 1972. Linkage of this cohort to the Hawaii Tumor Registry resulted in the identification of 214 (mainly post-menopausal) incident cases of endometrial cancer for 1972-1986. An average of 37 cancer-free controls were matched to each case on month and year of birth and ethnicity. A case-control analysis, conducted in each 5-year birth cohort, revealed no clear association of endometrial cancer with weight, height or body mass at ages 10 to 29 years. However, positive associations with adult body weight and gain in body mass since 1942 were observed for women diagnosed at age 60 or older. This association with obesity was strongest in women whose body mass was below the median in 1942 and equal to or above the median in 1972. No association with body size was detected in women diagnosed before age 60. Parity, age at first birth and socioeconomic indicators for 1942 and 1972 did not confound the analysis. These findings suggest that obesity affects the late stages of endometrial carcinogenesis, and the possibility that one or more determinants of weight gain may be independently associated with endometrial cancer risk.
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PMID:Early-age body size, adult weight gain and endometrial cancer risk. 186 Jul 27

A case-control study of 268 patients with endometrial cancer and 268 population controls was conducted during 1988-1990 in Shanghai, China, to evaluate etiologic factors in a population whose risk had not been substantially altered by the use of exogenous estrogens. In spite of this, the major risk factors resembled those found in other studies. The risk of endometrial cancer was significantly elevated among nulligravidas (OR = 5.4, 95% CI = 2.0-14.6) and decreased with number of pregnancies (p less than 0.01). Late age at menopause was associated with increased risk, while early age at menarche was unrelated. Use of oral contraceptives for more than 2 years was associated with a reduction in endometrial cancer risk (OR = 0.4, 95% CI = 0.1-1.2), while short-term use of oral contraceptives and other methods of contraception were unrelated. Obesity was a strong predictor of risk, with women in the highest quartile of weight having 2.5 times the risk of those in the lowest quartile. In contrast to many other studies, cigarette smokers were at elevated risk (OR = 1.7, 95% CI = 0.9-3.0). Risk was also elevated among women reporting a history of gall-bladder disease, polycystic ovaries, menstrual symptoms, and non-estrogen hormone use.
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PMID:A population-based case-control study of endometrial cancer in Shanghai, China. 187 68

A case-control study was undertaken to evaluate the roles of obesity and body fat distribution in the etiology of endometrial cancer. The study also included an evaluation of the associations of serum estrone, estradiol, and androstenedione with obesity, body fat distribution, and endometrial cancer risk. The study included 168 cases and 334 control subjects identified at an optometry clinic. A strong, positive relationship between overall obesity and endometrial cancer was found. The relative rate of endometrial cancer for women in the upper 90th percentile of a body mass index compared to those below the median was estimated as 5.5 with 95% confidence limits of 3.2-9.6. There was no association between endometrial cancer and the waist to hip ratio, an index of upper versus lower body fat distribution. A statistical test of trend across the four quartiles of the waist to hip ratio yielded a P value of 0.45 after adjustment for confounding by the body mass index. On the other hand, there was a statistically significant, independent positive effect of a high subscapular to tricep skinfold ratio, a measure of central versus peripheral obesity, on endometrial cancer risk. The relative rates of endometrial cancer for the second, third, or fourth quartile compared to the first quartile of this index were 1.5, 1.9, and 2.7, respectively (P = 0.007), after adjustment for the body mass index. Serum estrone and estradiol, but not androstenedione, were statistically significantly correlated with the body mass index among control subjects (r = 0.37 and 0.40 for estrone and estradiol, respectively). On the other hand, each of the sex hormones was uncorrelated with the waist to hip ratio after adjustment for body mass. The correlations between each of the three hormones and the subscapular to tricep skinfold ratio among controls were weak and were not statistically significant (0.10, 0.10, and 0.14 for estrone, estradiol and androstenedione, respectively). Cases had statistically significantly higher mean serum estrogen and androstenedione levels than did controls and these elevations did not simply reflect a higher prevalence of obesity among them. The findings are equivocal with respect to fat patterns and endometrial cancer. We suggest that future epidemiological studies of cancer and body fat distribution more carefully distinguish among the various types of fat patterns.
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PMID:Endometrial cancer, obesity, and body fat distribution. 198 74

From July 1985 to January 1989, 133 patients underwent endometrial sampling for evaluation of post menopausal bleeding (PMB). Of these patients, 114 (85.7 percent) showed benign histology with an average age of 58.6 years. Nineteen (14.3 percent) were malignant, all of which showed endometrial carcinoma. The average age was 65. In addition, 26.3 percent of patients with carcinoma had higher grade of tumor at hysterectomy when compared with the preoperative biopsy. The average volume of tissue removed at curettage was significantly greater in those with carcinoma. Hormonal therapy, duration of symptoms, hypertension, obesity or diabetes were not significant risk factors for carcinoma in our series. PMB remains a major symptom that may predict endometrial carcinoma and must be evaluated. In those patients with carcinoma, intraoperative evaluation of the uterus for tumor grade and depth of invasion is important in determining the extent of surgery.
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PMID:Post menopausal bleeding as a risk factor for endometrial carcinoma. 199 92

The descriptive and analytical epidemiology of endometrial cancer is reviewed. Over the last few decades, age-standardized incidence rates have been rising in several countries. The rise has been even greater in terms of absolute numbers of cases, and hence public health implications, due to the aging of the population. Although endometrial cancer rates were found to be higher in richer countries and urban populations, there is now evidence of some changes in the socioeconomic determinants of the disease in developed countries. In etiological terms, any factor that increases exposure to unopposed estrogens (such as menopausal replacement treatment, obesity, and irregular menstrual cycles) tends to increase the risk of the disease, while factors that decrease exposure to estrogens or increase progesterone levels (such as oral contraceptives or smoking) tend to be protective. Less well defined, or more difficult to explain in biological terms, is the role of other factors, such as births, miscarriages, or diabetes and hypertension, and only suggestive evidence is available on diet from analytical epidemiology. The data reviewed herein are discussed in terms of models of carcinogenesis, as well as attributable risks and public health implications.
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PMID:The epidemiology of endometrial cancer. 202 52

The health risks of obesity increase with its severity and reach significance at a weight greater than 20% above optimal, by using life insurance tables, or at a body mass index greater than 27. Risks include hypertension, insulin resistance and diabetes mellitus, cardiovascular disease, hypertriglyceridemia, low high-density-lipoprotein cholesterol, and, in some studies, high total-and low-density-lipoprotein cholesterol. There is an increased mortality from endometrial cancer in women and from colorectal cancer in men. Chronic hypoxia and hypercapnia, sleep apnea, gout, and degenerative joint disease can occur with more severe obesity. The distribution of body fat is directly related to these health risks. Abdominal obesity is more dangerous than gluteal-femoral obesity because the amount of intraabdominal fat seems to determine much of the increased peril; therefore, risks of cardiovascular disease, stroke, hypertension, and diabetes increase with abdominal obesity, even independently of total fat mass.
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PMID:Health implications of obesity. 203 92


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