How Common Are Uterine Fibroids and Who Gets Them

Uterine fibroids are among the most common growths in people with a uterus, with a lifetime prevalence estimated at roughly 75% and a lifetime risk of clinical diagnosis exceeding 60% in women over 45.¹² Despite that staggering frequency, the condition is heavily shaped by race, genetics, hormones, and body composition, which means the experience of fibroids varies enormously from person to person.

The Gap Between How Many People Have Fibroids and How Many Know It

The true prevalence of fibroids is difficult to pin down because most of them cause no symptoms at all. At least half of fibroids are asymptomatic, and researchers suspect the real figure is higher because that estimate comes mostly from cases found by accident during unrelated exams like cervical screening.³ So the fibroids that never prompt a doctor visit, and never happen to show up on an unrelated scan, go uncounted entirely.

This detection gap helps explain why prevalence numbers vary so much depending on the study method. When researchers in a 2023 study used transvaginal ultrasound to screen a diverse community-based cohort of nearly 1,000 reproductive-age women, they found fibroids in about 20% of participants overall.⁴ An Australian data-linkage study that relied on hospital and outpatient coding found that only about 7% of women had a recorded diagnosis by their late forties.⁵ That gap between 7% and 20% and the lifetime estimate of 75% is not a contradiction. It reflects the difference between looking for fibroids with imaging, waiting for them to show up in medical records, and accounting for every fibroid that will ever develop over a full lifetime, including the ones that stay small and silent.

Who Gets Fibroids Most Often

Race and ethnicity are among the strongest predictors of fibroid development. In the community ultrasound study mentioned above, roughly 36% of Black or African American participants had fibroids, compared with about 22% of Asian-Chinese, 13% of Hispanic or Latina, and 11% of White participants. Black and Asian-Chinese women were disproportionately affected across all age groups.⁴ That three-fold difference between Black and White women is consistent across decades of research and holds up after adjusting for other factors like weight and income.

The disparity is not just about having fibroids. African American women tend to be diagnosed at younger ages, are more likely to have bothersome symptoms, and may respond differently to certain medical treatments than White women.⁶ The reasons are not fully understood, but they appear to involve a tangle of genetic susceptibility, differences in hormone metabolism, greater exposure to environmental chemicals in some communities, and disparities in healthcare access that delay diagnosis and limit treatment options.

Age matters too. Fibroids are rare before puberty and uncommon in the early twenties. They become increasingly prevalent through the thirties and forties, peaking in the years just before menopause. After menopause, existing fibroids tend to shrink, and new ones seldom develop. The age pattern tracks neatly with reproductive hormone levels, which is not a coincidence.

The Genetic Side

Fibroids clearly run in families. If your mother or sister had them, your own risk goes up. Researchers have identified several gene mutations that drive fibroid growth. Mutations in a gene called MED12, for instance, show up in a large share of individual fibroid tumors. Other genes, including FH, HMGA2, and COL4A5-COL4A6, have also been linked to fibroid development.⁷ These are typically somatic mutations, meaning they happen within uterine tissue over a person’s lifetime rather than being inherited at birth.

On the inherited side, large genome-wide studies have begun mapping the genetic landscape more precisely. A recent multi-ancestry meta-analysis identified several novel risk spots in the genome, including variants near genes involved in tumor suppression (TP53), cell structure (SYNE1), and cellular signaling (FOXO3 and VIP, among others).⁸ Some genetic loci also overlap with those that influence the age a person first gets their period, suggesting that the genetics of fibroid risk and the genetics of reproductive timing share common pathways.⁹

A rarer but striking example is hereditary leiomyomatosis and renal cell cancer, a syndrome caused by inherited mutations in the FH gene. Women who carry this mutation have roughly seven to eight times the odds of developing uterine fibroids compared with women who do not.¹⁰ This condition is uncommon, but it illustrates how powerfully a single genetic change can shift fibroid risk.

How Hormones and Reproductive History Shape Risk

Estrogen and progesterone are the central hormonal drivers of fibroid growth. Fibroids are studded with receptors for both hormones, and progesterone in particular promotes fibroid cell proliferation through multiple signaling pathways.¹¹ This hormonal dependence explains why fibroids grow during the reproductive years, why they can enlarge during pregnancy when hormone levels surge, and why they tend to shrink after menopause when those hormones drop off.

The age at which a person first menstruates appears to matter. Each additional year of delay in the onset of periods is associated with a measurable drop in fibroid risk, and the link is especially strong for developing multiple fibroids. The association holds for women of all racial backgrounds.¹² The working theory is straightforward: earlier periods mean more total years of hormone exposure, which gives fibroids more time and more biochemical fuel to develop.

Pregnancy, on the other hand, appears to be protective. Epidemiologic data consistently show that having given birth is associated with reduced fibroid risk, and each additional birth adds to the protective effect.¹³ One plausible explanation involves postpartum uterine remodeling, the rapid process by which the uterus shrinks back to its pre-pregnancy size. During that remodeling, small fibroids may get cleared out. A study that tracked women from early pregnancy to the postpartum period found that about 36% of women who started pregnancy with a single fibroid had no identifiable fibroid on the postpartum ultrasound, and most of the remaining fibroids had decreased in size.¹⁴

Body Weight, Metabolism, and Physical Activity

Higher body mass index is linked to greater fibroid risk, though the relationship is not a simple straight line. A prospective study found the association between BMI and fibroid incidence to be nonlinear, potentially driven by the effects of body fat on inflammation and hormone levels.¹⁵ Fat tissue produces estrogen on its own, which could feed fibroid growth independent of what the ovaries are doing.

Where fat accumulates seems to matter more than overall weight. Abdominal visceral fat, the deep fat surrounding internal organs, is more strongly linked to fibroids than fat stored under the skin. A case-control study found that a higher visceral fat area, waist-hip ratio, and body fat percentage were each associated with significantly elevated fibroid odds, with the waist-hip ratio showing the strongest association.¹⁶ Insulin resistance, a metabolic state common in people carrying excess visceral fat, has also been independently linked to fibroid risk in non-diabetic women.¹⁷

Physical activity works in the other direction. In a study that adjusted for BMI and other risk factors, women who exercised the most (roughly seven or more hours per week) were about 40% less likely to have fibroids compared with the least active women. The pattern held for both African American and White participants, and the protective association appeared to be with fibroid development itself rather than with slowing the growth of existing ones.¹⁸ Exercise likely helps by improving insulin sensitivity and lowering circulating estrogen levels, though the exact mechanism has not been fully worked out.

Environmental Exposures and Diet

A growing body of research points to endocrine-disrupting chemicals as a possible contributor to fibroid risk. These are synthetic chemicals that can interfere with hormone signaling. Certain phthalates, particularly a group derived from DEHP (commonly found in plastics, food packaging, and personal care products), have been linked to increased uterine volume in women already being treated for fibroids. In one study, a doubling of urinary DEHP metabolite levels was associated with a roughly 33% increase in uterine volume.¹⁹ Bisphenol A (BPA) and certain ultraviolet-filter chemicals found in sunscreens have also been detected at higher concentrations in women with fibroids, although after adjusting for other variables, those associations did not reach statistical significance in at least one study.²⁰ The field is still evolving, but reviews of both human and lab studies suggest endocrine disruptors may contribute to fibroid risk and progression through epigenetic changes that alter how genes are expressed.²¹

Dietary factors have received attention too, though the evidence is messier. The association between red meat and fibroid risk, for example, appears significant in some populations (such as Italian women) but not in others (such as Chinese women).²² Vitamin D insufficiency has attracted the most consistent interest; multiple studies have observed lower blood levels of vitamin D in women with fibroids, though it remains unclear whether low vitamin D plays a causal role or simply tags along with other risk factors like darker skin pigmentation and higher BMI.²³ For fiber, vitamin C, vitamin E, and phytoestrogens, reviews have found no clear association with fibroid risk.

What Happens at Menopause

Because fibroids depend on reproductive hormones, menopause generally acts as a natural brake. Existing fibroids tend to shrink as estrogen and progesterone levels fall. A retrospective study that monitored nearly 100 women annually for up to ten years after menopause found that fibroids shrank most rapidly in the first two years, with the rate of decrease slowing considerably after that.²⁴ That early burst of shrinkage aligns with the steepest drop in hormone levels during the menopausal transition.

But “fibroids shrink after menopause” is a generality, not a guarantee. Some fibroids persist well into the postmenopausal years, and in rare cases they can continue to cause symptoms.²⁵ Hormone replacement therapy can maintain or even boost estrogen levels enough to sustain fibroid growth after natural menopause. So for women considering menopausal hormone therapy who also have known fibroids, monitoring is usually recommended.

Fibroids, Fertility, and Pregnancy Complications

Whether fibroids affect your ability to conceive depends heavily on where they sit in the uterus. Submucosal fibroids, those that bulge into the uterine cavity, are the most likely to interfere with implantation and have been linked to recurrent pregnancy loss; removing them improves pregnancy rates. Fibroids that grow on the outer surface of the uterus (subserosal) do not appear to affect fertility at all. Intramural fibroids, which grow within the muscular wall, seem to reduce fertility to some degree, but the evidence on whether removing them helps is still unclear.²⁶

During pregnancy, roughly 10% to 30% of women with fibroids experience complications. The most common pregnancy-specific issue is red degeneration, a painful condition where a fibroid outgrows its blood supply, occurring in about 8% of pregnant women with fibroids.²⁷ A large meta-analysis found that after adjusting for other factors, fibroids were associated with higher rates of preterm birth, cesarean delivery, placenta previa, placental abruption, postpartum hemorrhage, breech presentation, and preeclampsia. Larger fibroids carried a greater risk for complications like breech presentation and postpartum hemorrhage than smaller ones did.²⁸ Still, the majority of pregnancies with fibroids proceed without serious problems, and many people are never even aware of a fibroid during pregnancy until a routine ultrasound spots one.

The Mental Health and Quality-of-Life Toll

The burden of symptomatic fibroids extends well beyond heavy bleeding and pelvic pain. Qualitative research with women who have fibroids has found widespread emotional distress, including fear, anxiety, anger, and depression. Many women describe feeling that they have no control over their condition, and some report a negative self-image that affects intimacy and relationships.²⁹ The distress has been compared in severity to what people with other chronic diseases experience.³⁰

A large cohort study quantified the link more precisely: women with a fibroid diagnosis had higher rates of depression and anxiety than those without, and the association was stronger among women who also had heavy menstrual bleeding or pain symptoms. Women with fibroids who ultimately underwent hysterectomy had even higher rates of depression and anxiety compared with fibroid patients who did not have surgery, and a notably elevated rate of self-directed violence.³¹ These findings do not mean fibroids or hysterectomy directly cause psychiatric illness, but they underscore that the condition sits inside a web of physical symptoms, treatment stress, and emotional strain that clinicians and patients often underestimate.

Treatment Disparities and Economic Costs

Who gets fibroids and who gets access to the best treatment are not the same question, and the gap is troubling. A systematic review found that Black women faced higher odds of receiving open hysterectomy rather than less invasive procedures, spent longer in the hospital, and had more perioperative complications compared with White women.³² Even after controlling for age, insurance type, and year of surgery, race, income, education, and whether a patient lived in a rural area were each independently associated with receiving more invasive treatment. Black patients, lower-income patients, those with less education, and rural patients all had a higher predicted probability of ending up with the most invasive surgical approach.³³ Uninsured women and patients on Medicaid are also less likely to receive minimally invasive procedures, partly because of geographic access to hospitals that offer them.³⁴

The economic footprint of fibroids is substantial. An early cost analysis estimated that fibroids cost the U.S. somewhere between $5.9 billion and $34.4 billion annually when combining direct medical costs with lost work productivity.³⁵ A more recent comparative analysis placed the lost-work costs alone at $6.4 to $17.9 billion in 2022, with the largest chunk attributable to lost productivity around hysterectomy.³⁶ Across five European countries, about a third of employed women with a fibroid diagnosis reported missing work, and overall worker productivity was reduced by roughly 36%.³⁷ These numbers reflect a condition that, despite being labeled “benign,” carries a serious societal cost driven largely by delayed diagnosis, limited treatment options, and the outsized toll on the workforce when hysterectomy remains the default surgical solution.

Animal Models and Why Fibroid Research Is Hard

One reason fibroids remain poorly understood relative to their prevalence is that they are difficult to study in the lab. Humans are one of very few species that develop uterine fibroids spontaneously, which limits what researchers can learn from standard lab animals. Most fibroid research relies on rats and mice, using methods like hormonal injections, genetic engineering, chemical exposures, or transplanting human fibroid tissue into immunocompromised animals.³⁸³⁹ Each approach captures some aspect of fibroid biology but none fully replicates the human condition, which means therapies that look promising in animals sometimes fail to translate. This research bottleneck helps explain why treatment options for fibroids have evolved more slowly than for many other common conditions, and why hysterectomy still accounts for such a large share of the economic burden despite being the bluntest possible intervention.