Uterine fibroids are a common non-cancerous condition affecting an estimated 70% to 80% of women by age 501 . These growths can cause pain, heavy menstrual bleeding, and fertility problems, significantly impacting quality of life2 . Recent research suggests that high blood pressure, or hypertension, is linked to an increased risk of developing uterine fibroids, while treatment of hypertension with medication may reduce this risk1 2. Understanding this connection could open new avenues for prevention and management of fibroids in midlife women.
New research finds a link between high blood pressure and uterine fibroids in midlife women. Treating high blood pressure could play a role in preventing fibroids, which affect up to 80% of women by age 50. Untreated hypertension increases fibroid risk, while antihypertensive medication, especially ACE inhibitors, lowers it significantly1 24.
Hypertension Drugs and Fibroid Risk Reduction
A large cohort study involving 2,570 midlife women followed from 1996 to 2013 found that hypertension is a significant risk factor for uterine fibroids3 . Women who developed new-onset hypertension during the study had a 45% higher risk of being diagnosed with fibroids compared to those with normal blood pressure3 4. Untreated hypertension was associated with a 19% increased fibroid risk, while women treated for hypertension had a 20% reduced risk compared to normotensive women3 4.
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Uterine fibroids affect up to 80% of women by age 50, and treating high blood pressure may help reduce fibroid risk1 .
Among antihypertensive medications, angiotensin-converting enzyme (ACE) inhibitors showed the strongest association with reduced fibroid risk. Hypertensive women using ACE inhibitors had a 48% lower chance of developing uterine fibroids compared to untreated hypertensive women3 54. Beta blockers also demonstrated a protective effect, reducing fibroid incidence by 15% in hypertensive women, particularly in those aged 30 to 396 .
The renin-angiotensin-aldosterone system (RAAS), which regulates blood pressure and fluid balance, may play a key role in this relationship. Activation of RAAS releases hormones that can bind to uterine fibroid cells and promote their growth7 . ACE inhibitors block this system, potentially limiting fibroid development by reducing the hormonal stimulation of fibroid cells3 57.
“Very little is known about how and why fibroids develop and grow in women. This is frustrating because the current treatment options for fibroids are limited and we don’t know how to prevent them.”
— L. Elaine Waetjen, UC Davis Health1
Other factors influencing fibroid risk include obesity, which was present in about 25% of the study participants and is a known risk factor for fibroids3 . The study’s reliance on self-reported data and the specific characteristics of the cohort may limit the generalizability of the findings3 .
Key findings from the cohort study:
- New-onset hypertension increased fibroid risk by 45% 3
- Untreated hypertensive women had a 19% higher fibroid risk3
- Treated hypertensive women had a 20% lower fibroid risk than normotensive women3
- ACE inhibitor use was linked to a 48% reduction in fibroid development odds5
- Beta blockers reduced fibroid incidence by 15%, especially in women aged 30–396
- About 25% of participants were obese, a significant fibroid risk factor3
Investigation into mechanisms and health implications is warranted; if the associations are causal, antihypertensive medication use where indicated may present an opportunity to prevent clinically apparent fibroid development at this high-risk life stage2 .
Can Blood Pressure Medicine Prevent Fibroids?
While the association between hypertension and fibroid risk is clear, it remains uncertain whether blood pressure medications can directly prevent or treat uterine fibroids3 . The current evidence shows correlation but does not prove causation3 9. The biological mechanisms by which antihypertensive drugs might influence fibroid growth are still under investigation3 .
The RAAS pathway is a promising target. Hormones released by RAAS activation can stimulate fibroid cell proliferation, and ACE inhibitors may reduce this effect by blocking RAAS activity7 . However, the timing, dosage, and long-term impact of these medications on fibroid development have not been fully established3 .
Fibroid growth is also influenced by other factors such as progesterone pathways and inflammation, which complicate the therapeutic landscape10 7. High blood pressure may cause inflammation and damage to blood vessels and uterine muscle cells, potentially promoting fibroid growth4 .
“Current clinical practice recommends that patients have their blood pressure checked at every clinical visit because controlling high blood pressure is necessary to lower the risk of heart disease and stroke, which are life-threatening.”
— Susanna Mitro, PhD, Kaiser Permanente Division of Research4
Lifestyle factors that reduce hypertension risk may also lower fibroid risk. These include regular exercise, a diet rich in fruits and vegetables and low in red meat, and maintaining a healthy weight4 .
Summary of current understanding:
- No clinical evidence yet confirms that blood pressure medication prevents fibroids in women without hypertension9
- ACE inhibitors may inhibit fibroid growth by modulating RAAS-related hormonal pathways7
- Beta blockers may offer dual benefits by controlling hypertension and reducing fibroid risk6
- Fibroid pathogenesis involves multiple pathways including hormones and inflammation10 7
- Lifestyle changes that lower blood pressure may also reduce fibroid risk4
