By: Beth Walsh for Fibroids1Numerous efforts are underway to learn what causes uterine fibroids and what can be done to prevent them. Fibroids are non-cancerous tumors that develop from the myometrium (smooth muscle layer) of the uterus. Fibroids are said to affect up to 75 percent of reproductive-age women, and approximately 25 percent of these experience symptoms. Several researchers are studying the effect of the environment on the development of these benign tumors.
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Fibroids only need to be treated if they are causing symptoms. Call your doctor if you notice any of the following: abnormal or heavy bleeding, pelvic pain, painful intercourse, difficulty emptying your bladder, and difficulty moving your bowels.
The primary treatment for patients with large or symptomatic fibroids is surgery. Hysterectomy (surgical removal of the entire uterus) is the most common technique used to treat this disorder, with fibroids being the reason for about one-third of all hysterectomies in the United States, or about 200,000 procedures a year.
However, there are less invasive options – such as uterine fibroid embolization – available to you as well. Be sure to talk over your options with your doctor. |
A 2006 status report from the National Institutes of Health provides a lengthy summary of uterine fibroid research. Among the environmental studies, one proposes that uterine smooth muscle tumor cells closely resemble normal uterine smooth muscles cells during pregnancy, but have escaped controls that cause these cells to regress or die. The pregnancy-like phenotype allows these cells to proliferate in response to estrogens, estrogen-like compounds, and other environmental cues. For whatever reason, they don’t regress or die when the uterus is removed. So far, studies on rats support this hypothesis; treatment of young rats with estrogenic compounds accelerated the growth of fibroids. Further, tumor incidence in aged rats is significantly reduced with multiple pregnancies and deliveries. An epidemiologic study confirmed that pregnancy is protective – and that prenatal exposure to diethylstilbestrol (DES) is associated with increased incidence of fibroids in adulthood.
Researchers at Vanderbilt University are looking at the relationship between environmental toxins and uterine gene expression. The investigators will run a series of experiments to examine mechanisms underlying “early” and “late” responses to estrogen. They propose to test the hypothesis that early responses – activities such as RNA transcription and the increase of blood flow in bodily tissues (hyperemia) – are estrogen-receptor independent, but that they initiate a series of events to prepare targets for the later estrogenic-dependent events, which include processes like DNA synthesis and mitosis, or duplication, of epithelial cells. Cooperation between these two responses is necessary for a full complement response in the uterus to natural or environmental sources of estrogen. Learning more about this early and late response crosstalk should help scientists better understand how fibroids develop.
At the University of Texas M.D. Anderson Cancer Center, researchers are working to understand the etiology of uterine fibroids at the molecular level and to determine how exposure to endocrine disruptors impacts their development. Working in a rodent model, scientists have found that those with a genetic predisposition to develop fibroids – and who are exposed to environmental estrogens at crucial times during development – have a dramatically increased risk of developing tumors later. This developmental reprogramming that disrupts tissue while it’s developing increases the risk of disease in adulthood.
