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

A relationship between exposure to exogenous estrogens and endometrial carcinoma has been reported in numerous studies. The incidence among those so exposed has been estimated to have been increased from 7.5 to 8 times that of those not exposed. Long-term therapy with estrogens for menopausal symptoms has been the usual history. Breast cancer patients treated with estrogens and young women taking sequential oral contraceptives have had increased risks. In this study, the records of Olmsted County, Minnesota, residents with endometrial uterine cancer diagnosed between 1945-1974 at the Mayo Clinic or at other medical facilities were reviewed. There were 122 adenocarcinomas and 23 adenoacanthomas. In 3 instances, adenocarcinomas contained zones of uterine sarcoma. For each of the 146 patients there were 4 age-matched controls. Estrogen use for 6 months or more was recorded for 39 (27%) of the 145 cases and for 163 (28%) of the 580 controls. The controls had more frequent histories of short-term estrogen therapy. Cancer patients had relatively more estrogen use for menopausal symptoms. The relative risk of endometrial cancer tended to increase with the duration of exposure to conjugated estrogens from 2.0 with any exposure to 4.9 (p less than .01) after 6 months or more and to 7.9 after 3 years or more. The risk increased with larger doses (1.25 mg or more) and with continuous administration of conjugated estrogen. Myometrial invasion was superficial in 77 cases and deep in 44 cases. Long-term use of conjugated estrogen was frequently associated with low-stage low-grade superficially invasive endometrial malignancy. The 5-year survival rate of the 145 patients was 85%. Patients with Stage 1 had a 95% relative 5-year survival rate. Those with Stages 2, 3, or 4 had 50% survival rates. Of other risk factors, obesity and nulliparity were noted. Patients had more frequent records of benign cystic adenoma and of adenomatous hyperplasia than controls. The corrected age-specific rate for endometiral cancer increased to a maximum of about 90/100,000 population per year in the group aged 55-64 and then diminished with age. An increase in endometrial cancer among those at risk may have been nullified by an increase in those who have had a hysterectomy. In this study the incidence of endometrial carcinoma in Olmsted County does not show an increase in the last 3 decades. It is noted that the long-term use of conjugated estrogens in this area has been relatively low.
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PMID:Exogenous estrogen and endometrial carcinoma: case-control and incidence study. 19 Aug 87

Estrogen replacement therapy is widely used to treat menopausal symptoms and prevent osteoporosis. The mechanism of these and other estrogen effects is currently under investigation. We studied the plasma steroid hormone and sex hormone binding globulin levels in frozen plasma obtained from 977 women aged 50 to 79 years from 1972 to 1974. Almost all of the 301 women who reported current use of noncontraceptive estrogen were taking conjugated estrogen by mouth; none reported use of a progestin. Women taking estrogen were significantly younger, thinner, and more likely to smoke cigarettes than women not taking estrogen. Sex hormone binding globulin and all endogenous hormones except testosterone were negatively correlated with age; estradiol was positively and cortisol and sex hormone binding globulin were negatively associated with obesity. After adjusting for age and obesity, dehydroepiandrosterone sulfate, androstenedione, and free testosterone were significantly lower in women currently taking estrogen than in women not using estrogen. These differences were independent of cigarette smoking. As expected, estrogens (including free estradiol), sex hormone binding globulin, and cortisol levels were higher in treated than untreated women. The possibility that some of the benefits and risks of replacement estrogen are secondary to altered adrenal steroid metabolism and androgen levels needs further evaluation.
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PMID:Exogenous estrogen and endogenous sex hormones. 154 58

With our expanding knowledge of osteoarthritis (OA) over the years, our concept of this "aging" disease has been re-evaluated to that which is the opposite of traditional views. To clinicians and scientists, OA is no longer the inevitable disease of aging, as one conceptualizes gray hair. Epidemiological studies show a higher incidence of OA affecting polyarticular joints in women than age-matched men, particularly those over the age of 55. This discrepancy in sex difference in the OA incidence highlights the significance of sex hormones and their alterations in menopause. Evidence indicates that this alteration possibly occurs early in adult life and may well persist into menopause. As well, this hormonal perturbation is thought to be consequent to obesity in these women. Both in vivo and in vitro studies suggest that estrogen is chondrodestructive via the receptor-mediated mechanism. The finding of estrogen receptor in canine, rabbit, and human articular cartilage further confirms this hypothesis. Recent findings of elevated synovial estradiol level and higher estrogen receptor bindings in human osteoarthritic cartilage strongly suggest the importance of local uptake of estradiol (E2) and the possible up-regulation of estrogen receptors. Estrogen, like other hypothesized etiologies, is important in the development of OA in women.
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PMID:Osteoarthritis in women: its relationship to estrogen and current trends. 159 63

We report the fasting and post-challenge plasma insulin and glucose levels in 469 nondiabetic postmenopausal women from the Rancho Bernardo cohort according to the current use of estrogen replacement therapy. In these older women, the use of noncontraceptive estrogen was not associated with impaired glucose tolerance. Estrogen-treated women had lower levels of insulin than women who were not taking estrogen; these differences were not explained by age, obesity, or differential hormone use by women with known glucose intolerance. There were no significant differences in glucose and insulin levels in those taking conjugated equine estrogen (Premarin) alone compared to those taking it with medroxyprogesterone acetate (Provera).
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PMID:Ischemic heart disease risk in postmenopausal women. Effects of estrogen use on glucose and insulin levels. 216 81

Possible relationship of changes in food and nutrition situation in the period 1961-1985 with obesity were briefly outlined. More evidence, incl. methodological improvements of studies is needed to make definitive confirmation on DES vs. obesity.
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PMID:Comparison of dietary energy sources and obesity. 263 95

For examination of the effect of prior exogenous estrogen use on survival after diagnosis of endometrial cancer, 244 endometrial cancer cases newly diagnosed at North Carolina Memorial Hospital, Chapel Hill, North Carolina, between 1970 and 1976 were followed until 1982. Estrogen users (n = 46) were younger, had less advanced disease, and were more likely to be nonobese and white than were nonusers (n = 198). The estimated probability of surviving (Kaplan-Meier) five years after diagnosis was 0.89 for users and 0.53 for nonusers. When adjusted for age, grade, stage, obesity, race, and treatment (using the Cox proportional hazards regression model), the survival probabilities throughout the period of observation for estrogen users continued to be higher. The adjusted hazard rate for a nonuser was 2.05 (95% confidence interval (Cl) 0.96-4.39) times that for an estrogen user. The adjusted hazard rate from endometrial cancer only was 4.01 (95% Cl 1.22-13.21) times greater among estrogen nonusers. The more frequent occurrence of endometrial cancer in an earlier stage and grade among estrogen users may not be the sole cause of their lower hazard rate from this disease.
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PMID:The influence of exogenous estrogen use on survival after diagnosis of endometrial cancer. 366 33

Estrogen treatment of climacteric women has been found to be associated with a substantially increased risk of endometrial cancer and a possible slight excess risk of breast cancer. Numerous retrospective case-control studies, reported mainly in the United States, have provided evidence of a causal link between the use of estrogens and the development of endometrial cancer. The magnitude of the risk increase has been shown to be correlated with characteristics of the exposure, chiefly the duration of treatment and the presence of certain host factors in the patient, e.g. obesity and late menopause. Cases of endometrial cancer occurring after estrogen exposure were shown to have favorable tumor characteristics and excellent survival rates. The early results from a prospective cohort study have indicated that estrogen therapy, as practised in Sweden, is associated only with an excess risk of premalignant endometrial changes and that the addition of progestogens might exert a protective effect. The risk of breast cancer after estrogen therapy has been studied in both retrospective and prospective investigations. In the majority of these studies no evidence of an increased risk has been found. However, in two case-control and two follow-up studies the risk estimates were slightly but significantly raised in association with long-term and high-dose exposure.
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PMID:The risk of endometrial and breast cancer after estrogen treatment. A review of epidemiological studies. 385 77

Focus in this discussion of pulmonary embolism is on the following: risk factors (age, heredity and blood type, obesity, estrogen and oral contraceptive use/pregnancy, cardiovascular disease, cancer, and other risk factors); pathophysiology and presenting symptoms; laboratory procedures and findings (radiography, electrocardiography, lung scanning, and evaluation of lower extremity veins); treatment modalities (heparin therapy, thrombolysis, and surgery); and prevention. Pulmonary embolism may be the primary cause or a major contributory cause in as many as 200,000 deaths per year in the US. Most of these deaths occur in patients in whom the diagnosis is not suspected and, thus, not treated. The mortality rate for untreated pulmonary embolism is approximately 30%. 90% of patients survive the initial embolic event, but the correct diagnosis is made in no more than 2/3 of cases. Risk factors for the development of deep venous thrombosis are based upon the Virchow-Aschoff postulates, which include: trauma or disruption of the vein wall; stasis of blood flow in the veins; and increased coagulability of the blood. More than 85-90% of all pulmonary emboli originate from deep venous thromboses in the popliteal and femoral deep veins. Other important, although less frequent, sites of origin of venous thromboembolism include the pelvic veins, the renal and hepatic veins, the axillary veins in the upper extremities, and the right atrium. Accurate diagnosis and effective prevention and treatment depend on the clinician's awareness of risk factors for development of deep vein thrombosis. Estrogen may accelerate intimal proliferation in arteries and veins, and it may also increase permeability of venous vascular endothelium. The risk of thromboembolism increases as the dose of estrogen increases. Both pregnancy and oral contraceptive use significantly decrease venous tone and the velocity of blood flow in the calf of the leg. Appropriate treatment includes thrombolytic therapy for patients with massive pulmonary embolism, which results in hypotension or shock. Anticoagulant therapy with herapin followed by an oral anticoagulant is the primary treatment for most patients with submassive emboli in which there is less cardiovascular compromise. When thrombolytic therapy is used, it should always be followed by anticoagulant therapy. Prevention of primary or recurrent deep vein thrombosis is directed toward improving venous blood flow and reducing hypercoagulability.
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PMID:Pulmonary embolism: incidence, diagnosis, prevention, and treatment. 398 Feb 63

The efficacy of oral contraceptives (OCs) is influenced by any factor that affects circulating blood levels of exogenous estrogen or progesterone or that interferes with their action at a cellular level. Inadvertent pregnancies are not uncommon in combined pill users, and are usually due to errors of tablet taking. Estrogen-progestogen combinations work mainly by hypothalamic suppression; basal plasma levels of follicle stimulating hormone (FSH) and luteinizing hormone (LH) are usually repressed and their cyclical surges eliminated. Progestogen-only formulations have much less effect on central control and depend more on effects on the cervical mucus, endometrium, and possibly tubal function. Significant increases in FSH and LH levels may occur in the pill-free week among combined pill users. Reduction in dosage of some newer preparations appears to reduce the margin of error and, in low-dose progestogen-only pills, progestogen may reach inadequate levels for contraceptive effect before the expected time of the next pill. Higher failure rates in the 1st rather than in subsequent treatment cycles are mainly due to user failure, but method failures also may be more common, possibly because hypothalamic suppression increases over the 1st few cycles. 3 studies on pituitary and ovarian function in women who deliberately missed pills at specific stages showed an increase in breakthrough ovulation. Other clinical factors which may affect pill efficacy included vomiting, diarrhea, changing to a lower dose formulation, obesity, and drug interaction, especially with the antituberculosis drug rifampicin, some anticonvulsants, and antibiotics. Breakthrough ovulation from drug interaction is more likely to occur when OCs are administered early or late in the cycle. Analogously, the most hazardous times to miss pills are at the beginning or end of a monthly course.
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PMID:Why do inadvertent pregnancies occur in oral contraceptive users? Effectiveness of oral contraceptive regimens and interfering factors. 641 29

With few exceptions, most epidemiologic studies do not show an excess relative risk of breast cancer associated with menopausal estrogen therapy. Other studies show a relationship of breast cancer to obesity, which is characterized by increased endogenous estrogen production. This study explored the possibility of an interaction between ponderosity and exogenous estrogen use in a case-control study of 113 postmenopausal breast cancer patients and pair-matched hospital control subjects. In this series, neither menopausal estrogen use nor relative weight were significantly associated with breast cancer risk. However, among estrogen users, the relative risk of breast cancer was strikingly influenced by the ponderosity of the subjects; the relative risk was 0.41 for women whose relative weight was less than the median, compared with 1.29 for those whose relative weight exceeded the median. The mean age was also examined at diagnosis in order to explore the potential of exogenous estrogen as a tumor promotor. The mean age at breast cancer diagnosis in estrogen users, 58.1 years, was significantly lower than in nonusers, 63 years. A significant linear relationship was found between age at diagnosis and body weight among estrogen users. Estrogen-treated women in the lowest tertile of body weight had the diagnosis of breast cancer made seven years earlier than those in the highest tertile of weight. There was no significant difference in the distribution of clinical stages at diagnosis between estrogen users and nonusers. These data suggest that relative body weight is an important modifier of the effect of exogenous estrogens on breast cancer biology.
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PMID:Estrogen use and breast cancer. Interaction with body mass. 682 58


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