Endometriosis is an estrogen-driven condition, but what makes it unique is its ability to produce its own estrogen, creating a cycle that keeps the disease active. This self-sustaining estrogen production fuels inflammation, lesion growth, and symptoms like pain and bloating. Understanding how this happens can help in developing better treatment strategies.
How Endometriotic Lesions Create Their Own Estrogen
Unlike normal uterine tissue, Endometriotic lesions don’t rely solely on the ovaries for estrogen, they have their own mechanisms to produce and sustain it. Here’s how:
1. Aromatase Overproduction
Aromatase is an enzyme that turns androgens (hormones like testosterone) into estrogen. Normally, the uterus doesn’t make aromatase, but in Endometriosis, the lesions produce too much of it, creating extra estrogen. This feeds inflammation and makes lesions grow, worsening symptoms over time.
2. Inflammation Fuels Estrogen Production
Inflammation plays a key role in Endometriosis, and prostaglandin E2 (PGE2), a powerful inflammatory molecule that directly stimulates aromatase production. The more inflammation, the more PGE2 is produced, which triggers even more estrogen production. This creates a vicious cycle where inflammation and estrogen feed each other, making the disease progressively worse.
3. Estrogen Receptor Imbalance
Our bodies have two main estrogen receptors:
- Estrogen receptor alpha (ER-α) – Helps regulate estrogen activity.
- Estrogen receptor beta (ER-β) – Promotes estrogen activity.
In Endometriotic lesions, there is too much ER-β and too little ER-α, making the tissue highly sensitive to estrogen. This imbalance also makes the lesions resistant to progesterone, which is why many hormonal treatments don’t work as expected.
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In Endometriotic lesions, there is too much ER-β and too little ER-α, making the tissue highly sensitive to estrogen. This imbalance also makes the lesions resistant to progesterone, which is why many hormonal treatments don’t work as expected.
What Does This Mean for Treatment?
Since endometriotic lesions are capable of making their own estrogen, traditional hormonal treatments that simply suppress ovarian estrogen production may not be enough. Researchers are exploring targeted approaches, including:
- Aromatase Inhibitors (like letrozole) – These block aromatase and reduce estrogen production at the lesion level. They are not yet a standard treatment but show promise in certain cases.
- Surgical Excision – By removing estrogen-producing lesions, surgery can help break the cycle of self-sustaining estrogen production and inflammation.
- Anti-Inflammatory Approaches – Since inflammation and estrogen production are linked, treatments targeting inflammation may also help reduce estrogen levels.
By understanding how Endometriosis creates its own estrogen, we can move toward better treatments that break this cycle and bring lasting relief.