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

The metabolic mechanism for increased circulating free fatty acids in post-menopausal women with metastatic breast cancer was investigated. Hormone and metabolic response to glucose and growth hormone were compared to cancer patients and control subjects; thyroid, adrenal and pituitary function were evaluated. The results of these studies indicated that breast cancer patients had glucose intolerance and delayed and prolonged insulin secretion, increased basal growth hormone levels and insensitivity of adipose tissue to growth hormone. Cortisol and protein-bound iodine levels were normal and there was no lipolytic factor in the sera of breast cancer patients. The changes observed in breast cancer patients were not attributable to age, obesity, inanition or stress. These metabolic abnormalities may characterize host susceptibility to breast cancer or be effects of tumor.
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PMID:Metabolic parameters in women with metastatic breast cancer. 4 95

There is normally a layer of fat in the breast between the parenchyma of the breast and the skin. This is frequently thin and does not preclude the palpation of a tumor mass which involves the breast parenchyma. In patients suffering from obesity this fat pad becomes much thicker and obscures any underlying masses arising from the breast parenchyma. A case is reported in which a woman who was markedly obese lost a significant amount of weight and presented a bulge which was found to be carcinoma. This situation, in which fat obscures underlying breast lesion, has been observed in a number of patients. Attention is called to the limited value of physical examination of the breast in markedly obese patients. If any suspicion exists or if the patient is a candidate for cancer from a familial standpoint, mammograms are indicated.
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PMID:Obesity obscuring breast cancer: a case report. 19 Apr 79

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

The role of diet in the etiology of cancer of the breast and endometrium is considered. Geographic variation in rates, effects of migration, consequences of exogenous hormone use, and other epidemiologic factors are reviewed. Cancer of the endometrium is related to diet probably through simple caloric excess. The excess is reflected in obesity and the consequent overproduction of estrone, a natural but carcinogenic human estrogen. Diet may also influence breast cancer risk somewhat through the same mechanism. But this mechanism probably would not explain a large proportion of the disease. It is possible that, in addition, some specific dietary factor, for example, saturated fat, is causally related to breast cancer. Such a relationship would probably be mediated through an endocrine mechanism.
Cancer 1977 Jul
PMID:Diet and cancer of endocrine target organs. 19 11

At the Wilford Hall U.S. Air Force Base Medical Center, Texas, about 4000 postmenopausal women received estrogen replacement therapy during 1975. Of these, 2700 took estrogens only and 1240 were given a progestogen along with estrogen. Hysterectomy had been done previously on 1700 patients (42%), leaving 2300 with intact uteri and a risk of endometrial cancer. Adenocarcinoma of the endometrium was diagnosed in 7 patients. Of these, 6 had received estrogen therapy. There was 1 endometrial malignancy in a patient also receiving a progestogen. Among 510 untreated postmenopausal women with intact uteri, 1 adenocarcinoma of the endometrium was found. Type and dosage of estrogen were unrelated to endometrial malignancy. In addition to the 7 endometrial cancers from the clinic, 22 cases were diagnosed elsewhere and referred for treatment, 11 of these had received no hormones. 10 were taking estrogens and 1 was receiving Oracon for birth control. The incidence of endometrial malignancy in the U.S. is reported to be 21/100,000 women/year. There is a 3-fold to 9-fold increased risk of endometrial cancer associated with obesity alone. The probability that untreated postmenopausal women with intact uteri will develop carcinoma of the endometrium is 1/1000/year. With estrogen users, it is reported to be increased -7.6/1000 women/year. In the author's clinic during 1975, the incidence among those receiving only estrogen was 4.7/1000. Among those also receiving a progestogen the incidence was .8/1000. Unopposed estrogens apparently have a role in the etiology of endometria hyperplasia and neoplasia through incomplete shedding of the endometrium. Progesterone produces more complete sloughing of the endometrium and also converts all degrees of hyperplasia into secretory endometrium. Nulliparity, infertility, and anovulation are predisoposing factors to endometrial carcinoma. Progestogens are palliative therapy for endometrial cancer.
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PMID:Estrogens, progestogens and endometrial cancer. 19 79

Guidelines for perimenopausal hormone therapy are listed in outline form. Various symptoms of metabolic changes, of changes in the balance of the neurovegetative system, and of nervous system influences related to social and cultural factors can be treated with substitutive hormone treatment during menopause. Special considerations apply to women who have undergone ovariectomy. Cyclical estrogen treatment should be used, and gestagens should be given in addition to estrogens. In prescribing hormone therapy, all absolute and relative contraindications should be considered. Obese women should be on a strict diet during therapy, and smoking should be stopped. In the case of irregular bleeding, curettage should be performed to exclude the possibility of malignant cancer. The patient should have regular checkups to determine if possible side effects are of a serious nature. Types of medications and treatment regimens for menopausal women, for treating women who have or have not undergone ovariectomy, and for treating menopausal disorders are listed.
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PMID:[The treatment of women with climacteric symptoms with emphasis on perimenopausal hormone therapy]. 22 71

The original conception of the hypothalamus controlling feeding by the activity of two specific and reciprocally inhibitory centers has now been largely abandoned. Detailed neural research using a wide variety of methods has demonstrated the complex morphological and functional organization of this part of the brain and has modified the earlier simplistic approach. However, examination of the feeding responses to a variety of stimuli that represent components of control of feeding indicates that much or even most feeding control is extrahypothalamic. As demonstrated by the obesity or aphagia resulting from hypothalamic damage or from reversible hypothalamic interference, the hypothalamus influences or modulates feeding control, possibly by an enabling action, but it does not itself substantially control food intake either in the short or the long term. In the cachaxia of cancer, which can tentatively be regarded as a negative obesity, and which is closely reproducible in a rat model, the decline of food intake can be attributed to failure of control components that are all extrahypothalamic, and the deterioration of control of feeding appears to be quite independent of the hypothalamus. The very detailed reconstruction of intrahypothalamic circuitry that has been developed in recent years has not yet had any real impact on the problem of where or how the active control of food intake is generated or the way in which the hypothalamus influences this control.
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PMID:The hypothalamic syndrome in rats. 32 49

There is a need for reeducation of the population, especially in developed countries, as to the value of cereals in the diet. Cereals provide calories and important nutrients to the diet. Refined cereal products and unrefined cereals have certain advantages and disadvantages. With refinement, some nutrients and fiber are removed, but the body is better able to make use of certain nutrients. Essential nutrients are being replaced through fortification to compensate for losses in processing. The high fiber content of unrefined cereal products is believed to aid in the prevention of certain diseases. Special dietary bakery products have been introduced for the treatment of conditions generally exacerbated by standard food items. The increased consumption of cereal products appears warranted as a means of decreasing the saturated fat and cholesterol consumption. Cereals and cereal products have been mentioned in connection with allergies, celiac disease, schizophrenia, obesity, dental caries, cancer, atherosclerosis, goiter, and diverticulosis. This review discusses the possible role of cereals in the prevention or cause of these health problems.
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PMID:The nutritional and physiological impact of cereal products in human nutrition. 33 51

A retrospective case-control hospital study of 785 Caucasian breast cancer patients and 2,231 age-stratified controls was conducted in New York City from 1969-1975. Patients were grouped by pre- peri- and postmenopausal status at diagnosis for the analysis to make a distinctive separation for variables showing a pre- and postmenopausal differential. Demographic characteristics were similar for cases and controls. Previously recorded hormone-related risk variables for this disease were largely confirmed for pre- and perimenopausal women, i.e., late age at first birth (greater than 25), premenstrual symptoms of breast swelling and premenopausal chills and flushes. Mother's history of breast cancer was also found to be a risk variable. Nulliparity was a risk factor only perimenopausally. No risk was foun for absolute height, weight or for obesity (Quetelet Index), prior breast diseases or previous usage of exogenous hormones of any type and no "protective" effect was found for multiparous women and for nursing. Perimenopausally diagnosed patients (menopause to 10 years after) were similar to premenopausally diagnosed women on most risk factors. Risk variables determined by this and other case-control studies cannot account for the magnitude of differences in the international incidence of breast cancer.
Cancer 1978 Jun
PMID:The epidemiology of breast cancer in 785 United States Caucasian women. 35 Mar 77

The factors that increase the risk of development of endometrial cancer are reviewed. Many of these conditions are frequently associated with an elevated production of estrone in peripheral (nonendocrine) tissues from circulating androstenedione. Elevated estrone production may occur in young, anovulatory or postmenopausal women whose ovaries secrete higher than normal amounts of androstenedione. Alternatively, conditions such as obesity and liver disease are associated with higher than normal rates of conversion of androstenedione to estrone, resulting in high estrone levels. Neither the exact tissue site(s) of conversion nor the normal function of this process has yet been established. Much less information concerning steroid hormone receptor measurements in endometrial cancer than in breast cancer is available. However, it seems certain that measurement of progesterone receptors will provide a useful guide in the selection of progestational therapy.
Cancer Res 1978 Nov
PMID:Steroid hormones and endometrial cancer. 35 36


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