Uterine fibroids (leiomyomas) are non-cancerous growths that develop within the muscle wall of the uterus. They are extremely common, affecting a large percentage of women during their reproductive years, though many never experience symptoms. A common question is whether fibroids consume the blood shed during menstruation, given the severe bleeding often associated with them. Fibroids require a robust blood supply to survive and grow, but they do not “feed” on the menstrual blood that leaves the body. This confusion stems from the intense relationship fibroids have with the body’s circulatory system and the heavy bleeding they cause.
The Role of Hormones and Blood Supply in Fibroid Growth
Fibroid growth is primarily driven by the reproductive hormones estrogen and progesterone, which signal the fibroid cells to proliferate. Fibroid cells possess a greater number of receptors for these hormones compared to normal uterine muscle tissue, making them highly responsive to hormonal fluctuations. This reliance explains why fibroids typically grow during the childbearing years and often shrink after menopause when hormone levels decline.
To support their expansion, fibroids must secure a dedicated network of blood vessels, a process known as angiogenesis. Fibroid tissue releases various growth factors, such as Vascular Endothelial Growth Factor (VEGF), which instruct the body to create new arteries. These vessels branch off the main uterine arteries and penetrate the fibroid mass, delivering necessary oxygen and nutrients.
The resulting vasculature that feeds the fibroid is often structurally irregular and disorganized compared to healthy uterine tissue. This abnormal blood vessel formation creates a high-flow environment, diverting a portion of the body’s arterial blood supply directly to the fibroid. This dedicated arterial supply, not menstrual blood, sustains the growth and survival of the fibroid tissue.
Addressing the Myth: Supply Versus Menstrual Blood
The idea that fibroids “feed” on menstrual blood misunderstands the fundamental difference between circulation and excretion. The blood supply sustaining the fibroid is arterial blood, rich in oxygen and nutrients, circulating continuously throughout the body. This arterial blood is the supply line necessary for any living tissue to grow and function.
Conversely, menstrual blood is composed of shed tissue from the endometrial lining, mixed with blood exiting the body. This is waste material the body is expelling. Fibroids, which are solid tumors made of muscle and fibrous tissue, cannot absorb or utilize this shed material for sustenance or growth.
The confusion is compounded because fibroids contribute to heavy blood loss, making it appear they are responsible for the excessive flow. However, the fibroid’s existence requires a continuous inflow of fresh, circulating blood from the body’s arteries, not the outflow of menstrual discharge. A procedure like uterine artery embolization confirms this dependence by cutting off the arterial supply, causing the fibroid to shrink.
Understanding Fibroid-Related Heavy Bleeding
Fibroids cause heavy menstrual bleeding, medically termed menorrhagia, through several distinct mechanical and physiological pathways. One major factor is the increase in the total surface area of the uterine lining, particularly with submucosal fibroids that bulge into the uterine cavity. A larger area of tissue must shed during menstruation, leading to a greater volume of blood loss.
The physical presence of fibroids within the muscular wall can also impair the uterus’s ability to contract effectively. The uterus normally contracts to compress blood vessels after the lining is shed, which helps stop the bleeding. When fibroids disrupt this muscular architecture, the uterus cannot clamp down properly, resulting in prolonged and heavier menstrual flow.
The abnormal vasculature associated with fibroids also contributes to the bleeding. The newly formed, disorganized blood vessels surrounding the fibroid may be fragile and prone to leakage. Fibroids stimulate the local production of factors that interfere with normal clotting processes, leading to a failure to control bleeding.