What Happens to Endometriosis After Menopause?

Endometriosis is a condition where tissue similar to the lining inside the uterus, known as the endometrium, grows outside of the uterus. These growths, often called lesions, can be found on organs such as the ovaries, fallopian tubes, and the outer surface of the uterus. It is a chronic, inflammatory disease impacting well-being. While there is no definitive cure for endometriosis, various treatments aim to manage its symptoms and progression.

The Role of Hormones in Endometriosis

Endometriosis is strongly linked to hormones, particularly estrogen. Endometriosis lesions are estrogen-dependent, their growth and activity influenced by fluctuating hormone levels. Just like the uterine lining, these misplaced tissues respond to hormonal signals during the menstrual cycle. They can thicken, break down, and bleed, but unlike menstrual blood, this tissue has no way to exit the body, leading to inflammation, pain, and the formation of scar tissue. This hormonal sensitivity explains why symptoms worsen during menstruation when estrogen levels are higher.

Endometriosis During and After Menopause

Menopause marks a natural decline in the body’s production of estrogen by the ovaries. This reduction in hormonal stimulation often leads to an improvement or resolution of endometriosis symptoms for many. With less estrogen circulating, endometrial-like lesions often shrink and become less active. This often results in a significant decrease in the chronic pain and other issues associated with the condition.

However, the experience of endometriosis after menopause is not universally the same for everyone. While a considerable number of individuals report a natural remission of symptoms, some may continue to experience discomfort. Symptoms generally reduce in severity and frequency, aligning with decreased hormonal activity. The body’s shift away from regular menstrual cycles and associated hormonal fluctuations often relieves cyclical endometriosis pain.

When Endometriosis Persists or Returns

Despite the general expectation of symptom improvement after menopause, endometriosis can sometimes persist or even return. One reason for this is the continued presence of endogenous estrogen production in some post-menopausal individuals. Adipose (fat) tissue, adrenal glands, and even the ovaries can continue to produce small amounts of estrogen, which may be sufficient to stimulate existing endometriotic lesions. This can maintain the activity of the condition even without regular menstrual cycles.

Hormone Replacement Therapy (HRT) is another factor that can lead to persistent or recurrent endometriosis symptoms. If HRT, particularly estrogen-only therapy, is used to manage menopausal symptoms, it can re-stimulate dormant endometriotic implants. This external supply of estrogen can cause the lesions to grow and become active again, leading to a return of pain and other symptoms. The type and dosage of HRT are therefore important considerations for individuals with a history of endometriosis.

Certain types of endometriosis may also behave differently and be more resistant to the hormonal changes of menopause. For instance, deeply infiltrative endometriosis, which penetrates deeper into tissues, or endometriomas (cysts on the ovaries), might not fully regress with declining estrogen levels. Pain can persist even after active lesions have become inactive due to nerve damage, adhesions, or scar tissue formed over years of inflammation. These non-estrogen dependent factors can cause ongoing discomfort independent of hormonal activity. In rare cases, malignant transformation of endometriotic lesions can occur in post-menopausal individuals.

Managing Endometriosis Post-Menopause

For individuals whose endometriosis persists or recurs after menopause, ongoing medical monitoring and symptom management are important. Treatment plans are often individualized, taking into account the specific symptoms and overall health. If Hormone Replacement Therapy is being considered for menopausal symptoms, careful evaluation is necessary.

Lower doses of HRT or combined estrogen-progestin therapy may be options, as the progestin component can help counteract the stimulatory effect of estrogen on endometriotic tissue. Non-hormonal strategies for pain management include various medications or physical therapies. In certain circumstances, surgical interventions might be considered. This may be for persistent, severe symptoms, to address complications, or if malignancy is suspected. Even if active lesions are no longer present, scar tissue and adhesions from prior endometriosis can cause ongoing pain, necessitating targeted management.