Large-scale studies have demonstrated that obesity increases the risk of developing some forms of cancer. The association between obesity and cancer may result from factors such as fat distribution or sex hormone levels. Studies have also shown a relationship between a high-fat, low-fiber diet and cancer risk. High estrogen levels and low progesterone levels are associated with an increased risk of endometrial cancer. Obesity is known to raise estrogen levels and may lower progesterone levels. Obesity may increase the risk of breast cancer, but the evidence is less clear, since factors, such as age, country of origin, body-fat distribution, and family history, also play a major role in determining breast cancer risk. Sex hormones, insulin, and nutritional factors are also involved in the etiology of breast cancer. The incidence of lung cancer is inversely related to body weight.
obesity cancer risk estrogen progesterone levels, high estrogen low progesterone endometrial cancer obesity, obesity breast cancer risk fat distribution hormones, insulin nutritional factors breast cancer etiology, body mass index cancer risk sex hormones, obesity endometrial cancer progesterone deficiency mechanism, high caloric intake cancer risk hormone levels, Deslypere obesity cancer sex hormone hypothesis, body fat distribution breast cancer risk factors, low fiber high fat diet cancer risk hormonal
PMID 7674913 7674913 DOI 10.1016/0026-0495(95)90316-x 10.1016/0026-0495(95)90316-x
Cite this article
Deslypere, J. P. (1995). Obesity and cancer. Metabolism: clinical and experimental, 44(9 Suppl 3), 24-27. https://doi.org/10.1016/0026-0495(95)90316-x
Deslypere JP. Obesity and cancer. Metabolism. 1995;44(9 Suppl 3):24-27. doi:10.1016/0026-0495(95)90316-x
Deslypere, Jean Paul. "Obesity and cancer." Metabolism: clinical and experimental, vol. 44, no. 9 Suppl 3, 1995, pp. 24-27.
Keywords
Body Mass Index, Breast Neoplasms/complications, Endometrial Neoplasms/complications, Female, Gonadal Steroid Hormones/metabolism, Humans, Lung Neoplasms/complications, Male, Neoplasms/complications, Obesity/complications/physiopathology, Risk Factors, Weight Loss, Gonadal Steroid Hormones
Glueck CJ et al., 2013·Metabolism: clinical and experimental
We determined whether simple, clinical information on late and early menarche could help identify adult women with metabolic syndrome (MetS) and oligomenorrhea. We carried out a 26-year prospective follow-up of 272 suburban schoolgirls from ages 5-22 to 30-46. Early menarche (≤10 years, 5.2% of girls) and late menarche (≥16 years, 6.7% of girls) were both associated with oligomenorrhea (≥42 days) in adulthood, 29% and 11%, vs. 5% for normal menarche (11-15 years), p=.004. Early menarche was characterized by high childhood BMI (LS mean±SE: 21.2 ±1.0 kg/m2) and by high childhood and adult MetS (15%, 36%). Girls with late menarche had the lowest childhood BMI (18.1±1.0), no childhood MetS, and the highest adult MetS (47%). Increasing age at menarche was associated with uniformly decreasing childhood BMI and MetS, but with a U-shaped pattern of BMI (p = .05), MetS (p=.008), and oligomenorrhea (p=.02) in adulthood. Change to MetS from median ages 13 to 38 was associated with early-late menarche (OR=3.11, 95% CI 1.37-7.07, p=.007). MetS in adulthood was associated with childhood MetS (OR=8.03, 95% CI 2.57-25.08, p=.0003) and with early-late menarche (OR =3.43, 95% CI 1.44-8.15, p=.005). Menarche age had a curvilinear ('U' shaped) relationship with MetS and oligomenorrhea in adulthood. Late menarche and early menarche are risk factors for adult oligomenorrhea, MetS, and cardiometabolic abnormalities. Girls with early (≤ age 10) and with late menarche (≥ 16) represent a group at high risk for adult cardiometabolic abnormalities and oligomenorrhea that is easily identifiable by physicians.
PCOSOpioid Tone and Insulin ResistanceNaltrexone Opioid BlockadePCOS Hyperinsulinemia
Hyperinsulinemia secondary to a poorly characterized disorder of insulin action is a feature of polycystic ovarian disease (PCOD). On the other hand, being generally admitted that opioids may play a role in glycoregulation and that opioid tone is altered in PCOD, an involvement of the opioids in determining the hyperinsulinemia of PCOD patients could be suggested. The aim of this study was to evaluate the effect of a chronic opioid blockade on insulin metabolism and peripheral insulin sensitivity in PCOD hyperinsulinemic patients. Twenty-three women with PCOD were studied. An oral glucose tolerance test (OGTT) and a clamp study were performed at baseline (during the follicular phase) and after 6 weeks of naltrexone administration (50 mg/d orally). Based on the insulinemic response to the OGTT, 16 women were classified as hyperinsulinemic and seven as normoinsulinemic. Naltrexone treatment significantly reduced fasting (P < .05) and area under the curve (AUC) (P < .02) plasma insulin levels only in the hyperinsulinemic group. Moreover, hyperinsulinemic patients showed similar C-peptide incremental areas after naltrexone treatment, whereas in the same patients the fractional hepatic insulin extraction calculated from the incremental areas of insulin and C-peptide was found to be increased after chronic opioid blockade by naltrexone. For peripheral insulin sensitivity, the hyperinsulinemic group showed significantly lower (P < .01) total-body glucose utilization (M) compared with the normoinsulinemic group. No change in the M value was found after treatment in both groups. These data suggest that the insulin sensitivity and hyperinsulinemia after an OGTT are two distinct deranged features of the insulin disorder of PCOD patients.
Since the isolation of the enkephalins five yr ago, there has been an explosive increase in knowledge concerning the effects of the opiates and opioid peptides. This review deals with the interactions of opiates with the endocrine system in rat and man. The opioid peptides have been demonstrated to exert a variety of effects on pituitary hormone secretion in rat and man. In the rat, opiates stimulate growth hormone, prolactin and ACTH release and inhibit the release of the glycoprotein hormones. In man, the physiologic role of the endogenous opiates appears to be involved predominantly in ACTH and gonadotrophin regulation. Opiate effects are mainly exerted at the level of the hypothalamus but further modulating effects may occur at the pituitary and at end-organs. Opiate-induced hormonal effects appear to be mediated through dopaminergic and/or serotonergic mechanisms. Recent studies have also suggested a possible local neuromodulatory role for the opioid peptides in the control of carbohydrate metabolism and reproductive processes.