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 26,365 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Predisposing factors to cervical cancer development are age, smoking, socioeconomical status, parity, and number of sex partners. Long-term oral contraceptive (OC) use and less than 50 mg estrogen dose have been weakly linked to increased cancer risk. Regular examination and switching to other contraception in case of cervical intraepithelial neoplasia is recommended. Estrogen in sequential pills (Ovacon) increases the risks of uterine cancer by affecting the mucosa. Predisposing factors are: absence of pregnancy (nulliparity), postmenopause, hypertension, and diabetes. Parity reduces the risk. The risk is reduced in combined pills and after use of 1 year. Protection is offered by the progesterone component for 10-20 years after cessation of use. Ovarian cancer is prevented by parity and OC use even 10 years later. High estrogen levels inducing frequent ovulation damage the ovaries. Promoting factors are: old age, avoidance of breast feeding, and overweight. Breast cancer promoters are 1st pregnancy in older age, early menarche, and no pregnancy at all. OC use under age 25 and before 1st pregnancy are significant risk factors. High progesterone levels are associated with increased mitotic activity in the breast. Rare benign fibrocysts can develop into breast cancer. OC use is connected to hepatoma development mainly estrogen-induced. Liver cancer was found twice as high in OC users. Hepatoma often ruptures causing hemorrhage. 8% of liver tumors are malignant with a survival rate of 50% of patients to 4.8 years. The possible association of OCs to skin melanoma and hypophysial tumors could not be confirmed. OCs regulate menstruation, reduce bleeding, protect against uterine and ovarian cancer, but cervical and breast cancers have been influenced by them.
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PMID:[The contraceptive pill and cancer]. 207 68

Previous work from this laboratory has shown that chronic administration of dexfenfluramine (DF) caused substantial weight loss in rats that were overweight 3-4 mo after ovariectomy (OVX), but not in OVX rats that were of normal weight, as a result of estrogen replacement. The present study was conducted to determine whether the enhanced weight loss in the former group is because of either overweight per se or an inhibitory effect of estrogen on DF. Starting either 0, 6, or 14 wk after OVX, when weight gain was zero, moderate, or near maximal, respectively, rats received a 12-day regimen of either estradiol or the oil vehicle and either DF (3 mg.kg-1.day-1 by osmotic minipump) or no drug. DF had no effect on either food intake or weight gain of groups treated during 0-2 wk after OVX but had significant anorectic and weight loss actions in groups treated 6-8 and 14-16 wk after OVX. Estrogen had a similar effect at all three times and in the 14-wk group produced an effect that was additive with that of DF. Measures of plasma glucose and triglycerides and adipose tissue lipoprotein lipase activity did not correlate with the effectiveness of the drug to promote weight loss.
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PMID:Dexfenfluramine: action with estradiol on food intake and body weight in ovariectomized rats. 230 35

Thirty-one women (mean age 35.4 +/- 8.5 yr) who were overweight were matched and randomly placed into either a control group (Con; n = 6), a diet-only group (D; n = 8), a diet+aerobic endurance exercise training group (DE; n = 9), or a diet+aerobic endurance exercise training+strength training group (DES; n = 8). After 12 wk, the three dietary groups demonstrated a significant (P </= 0.05) reduction in body mass, %body fat, and fat mass. No differences were observed in the magnitude of loss among groups, in fat-free mass, or in resting metabolic rate. The DE and DES groups increased maximal oxygen consumption, and the DES group demonstrated increases in maximal strength. Weight loss resulted in a similar reduction in total serum cholesterol, low-density lipoprotein cholesterol, and high-density lipoprotein cholesterol among dietary groups. These data indicate that weight loss during moderate caloric restriction is not altered by inclusion of aerobic or aerobic+resistance exercise, but diet in conjunction with training can induce remarkable adaptations in aerobic capacity and muscular strength despite significant reductions in body mass.
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PMID:Physiological adaptations to a weight-loss dietary regimen and exercise programs in women. 921 73

This article discusses the risk factors for coronary heart disease (CHD)--the leading cause of death in the US--in women. Studies have shown that cigarette smoking more than doubles CHD incidence and increases CHD mortality by 70%. A cohort study among more than 121,000 female nurses in the US revealed that the risk of CHD was 6 times greater in heavy smokers than nonsmokers. The level of blood cholesterol is also a strong risk factor for CHD: levels of high-density lipoprotein (HDL) cholesterol are inversely associated with the risk of CHD. Thus, lowering low-density lipoprotein (LDL) and increasing HDL cholesterol levels reduce CHD risk in both men and women. Hypertension is a risk factor which responds well to pharmacologic treatment, and increasing levels of physical activity were proven to decrease CHD risk in numerous studies. Meanwhile, obesity, which is prevalent in the US, worsens other coronary risk factors such as hypertension, diabetes, and hypercholesterolemia. A study showed that overweight women (body mass index values 29) are at 3 times the risk for CHD as those with body mass index values less than 21. Diabetes mellitus is another CHD risk factor which is stronger in women than in men, and CHD death rates are 3-7 times greater among diabetic than nondiabetic women. Other studies revealed that women who consumed alcohol in moderation (10-15 g of alcohol per day) had a 40% lower risk of CHD compared with nondrinkers. There is a significant relationship between combined oral contraceptive and cigarette use and increased risk of CHD. Estrogen replacement therapy, low-dose aspirin, and antioxidant vitamins have been proven in studies to reduce the risk of CHD in women.
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PMID:Risk factors for coronary heart disease in women. 950 75

Although the mortality and incidence of cervical cancer have been decreasing, those of uterine-body, or endometrial, cancer have been increasing. The proportion of endometrial cancer was reported to have become 33.6% of primary uterine cancers in 1995. Infection with certain types of human papilloma virus (HPV) is considered to be etiologically important for the occurrence of cervical cancer. Because HPV is sexually transmitted, some risk factors for cervical cancer are associated with certain kinds of sexual behavior such as a young age at first intercourse, multiple partners, and infrequent use of barrier-type contraceptives such as condoms. Frequent conceptions and deliveries and histories of sexually transmitted diseases like infection with herpes simplex virus type 2 or chlamydia also have been suggested to be associated with the risk of cervical cancer. Smoking habits and infrequent intake of vegetables and fruits may be related to the increased risk of cervical cancer by supporting persistent infection of HPV through impaired immunological function. Although host factors such as a variant of a tumor suppressor gene like p53 have been assessed in terms of the risk of cervical cancer, these are not yet clearly elucidated. Estrogen stimulation of the endometrium unopposed by progesterone stimulation, namely, unopposed estrogen stimulation, is thought to be involved in the etiology of endometrial cancer. Frequent intake of animal fat, obesity or being overweight, infertility, and histories of diabetes mellitus, hypertension, and polycystic ovary syndrome have been reported to be risk factors for endometrial cancer, and they are thought to increase unopposed estrogen stimulation. Estrogen replacement therapy for postmenopausal symptoms, tamoxifen therapy for breast cancer, and taking sequential-type oral contraceptives have been shown to be exogenous risk factors for endometrial cancer in that they increase unopposed estrogen stimulation to endometrium.
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PMID:[Recent progress in epidemiologic research of uterine cancer]. 1124 42

Postmenopausal women with estrogen deficiency are at high risk for osteoporosis. Estrogen therapy has been shown to be effective in preventing postmenopausal bone loss and maintaining bone mineral density. The increasing number of women at risk for osteoporosis and the high cost of treating this condition emphasizes the importance of preventing osteoporosis. This study was designed to identify trends and predictors of estrogen use for osteoporosis prevention among postmenopausal women. A retrospective, cross-sectional study was conducted using Behavioral Risk Factor Surveillance System data (1997-1999). Women 35 years and older who had passed menopause or were currently going through menopause were identified from the states including the BRFSS module that asked questions about estrogen use. Results showed an increasing prevalence in estrogen use from 1997 to 1999 for osteoporosis prevention. In 1999, almost a third of the postmenopausal women surveyed used estrogen to prevent osteoporosis. Prevalence was higher among women 45-64 years of age, whites, and those with higher education levels. Physician counseling on the benefits and risks of estrogen therapy was the strongest predictor of estrogen use for prevention of osteoporosis. Insurance coverage and compliance with other preventive behaviors such as mammograms and Pap smears were also strongly associated with greater estrogen use. However, women who were at risk for acute drinking, not married, overweight or obese, and diabetic were all less likely to receive estrogen therapy for osteoporosis prevention. The relationships demonstrated between estrogen use and demographic characteristics, lifestyle behaviors and health care access and utilization factors underline the importance of targeting specific groups of women for promoting its protective effect against osteoporosis.
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PMID:Developing profiles of postmenopausal women being prescribed estrogen therapy to prevent osteoporosis. 1223 32

Overweight and abdominal obesity increase mortality risk, although the risk may be mediated by traditional cardiac risk factors. The authors assessed the association of baseline measures, change in overall body weight and abdominal obesity (waist circumference), and weight and waist circumference cycling with total mortality among postmenopausal women with known heart disease. They used data from 2,739 US women who participated in the Heart and Estrogen/progestin Replacement Study between 1993 and 2001. Over 6.8 years of follow-up, 498 women died. In adjusted Cox models that included either baseline waist circumference or body mass index (BMI), each was associated with mortality. However, after further adjustment for diabetes, hypertension, and lipoproteins, these associations disappeared. In models including both waist circumference and BMI, larger waist circumference (hazard ratio=1.40 per standard deviation, 95% confidence interval: 1.16, 1.68) was associated with increased risk and higher BMI (hazard ratio=0.81 per standard deviation, 95% confidence interval: 0.67, 0.97) was associated with decreased risk of total mortality, independent of cardiac risk factors. Weight and waist circumference cycling were not associated with mortality. Results show that both BMI and waist circumference are associated with mortality among postmenopausal women with established heart disease, but waist circumference may be more important than BMI, and their effects may be largely mediated by other cardiac risk factors.
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PMID:Association of total and central obesity with mortality in postmenopausal women with coronary heart disease. 1465 1

Obesity is increasing worldwide. Estrogen protects female mice from gaining weight in contrast to ovariectomy. Excess weight can inhibit wound healing. We determine the effects of obesity on wound healing in the presence and absence of estrogen. For this purpose, we generated (ovariectomized (OVX) and non-ovariectomized (NOVX)) lean mice by feeding a 30% calorie-restricted diet (CR), overweight mice a low-fat (LF) diet and obese mice a high-fat (HF) diet. CR mice had the lowest, LF an intermediate, and HF mice the highest body weights. OVX exacerbated weight gain in female mice. Wounds healed fastest in CR mice regardless of estrogen status. Contrastingly, wound healing in OVX obese female mice was delayed. In sum, OVX increased the propensity of gaining weight, CR mice healed wounds more rapidly than obese mice irrespective of estrogen status, and obesity in the absence of estrogen impaired wound healing.
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PMID:Obesity impairs wound healing in ovariectomized female mice. 1956 84

The risk of developing breast cancer and fatty liver is increased by alcohol consumption. The objective of the present study was to determine if obesity and exogenous estrogen supplementation alter the effects of alcohol on mammary tumorigenesis and fatty liver. Ovariectomized female mice were (1) fed diets to induce overweight and obese phenotypes, (2) provided water or 20% alcohol, (3) implanted with placebo, low- or high-dose estrogen pellets and (4) injected with Met-1 mouse mammary cancer cells. Alcohol-consuming mice were more insulin sensitive and developed larger tumors than water consuming mice. Obese mice developed slightly larger tumors than control mice. Alcohol consumption and obesity increased growth factors, hepatic steatosis, activation of Akt, and inhibited the caspase-3 cascade. Estrogen treatment triggered the loss of body fat, induced insulin sensitivity, suppressed tumor growth, reduced growth factors and improved hepatic steatosis. Results show that the effects of alcohol on mammary tumor and fatty liver are modified by obesity and estrogen supplementation.
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PMID:Estrogen inhibits the effects of obesity and alcohol on mammary tumors and fatty liver. 2185 Mar 68

Prostate problems, such as benign prostatic hyperplasia, prostatic intra-epithelial neoplasia, prostatitis, and prostate cancer have been recognized as problems largely related to androgens and genetic factors. They affect a large fraction of the elderly population, contributing significantly to morbidity and mortality. Estrogen has also now been recognized as one of the important regulators of prostate growth. Diet, general health, and obesity were disregarded as the causative or complicating factors until very recently. Increasing episodes of prostate problems, complications in overweight/obese individuals, or both have attracted attention toward these contemporary risk factors. Prostate problems are reportedly less frequent or less severe in areas in which a plant-based diet is predominant. Consumption of certain fatty acids, particularly of animal origin, has been correlated with increased prostate problems. As adipose tissue is increasingly being regarded as hormonally active tissue, high body fat and obesity need in-depth exploration to understand the associated risk of prostate problems. Adipose tissue is now known to affect circulating levels of several bioactive messengers and therefore could affect the risk of developing prostate problems in addition to several other well-recognized health problems. Nevertheless, increased plasma volume, excess tissue growth, and fat deposition could affect resection and number of biopsies required, thus adding further complications because of a delayed diagnosis. In short, evidence is gathering to support the influence of diet and obesity on prostate health. In this review article, we have tried to make this connection more apparent using supporting published data.
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PMID:Diet, obesity, and prostate health: are we missing the link? 2232 23


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