Endometrial Hyperplasia

Endometrial hyperplasia is an overgrowth of the endometrium, the lining of the uterus. It forms when estrogen acts on the lining for a long time. Progesterone is too low to balance that estrogen.

The glands in the lining multiply and crowd together. The most common sign is abnormal bleeding from the uterus.

Atypical hyperplasia (endometrial intraepithelial neoplasia, or EIN) is one form. It is the direct precursor of cancer of the lining (endometrial adenocarcinoma).

One long-term study followed women whose hyperplasia was never treated. It tracked them for an average of 13.4 years. Cancer developed in 8% of women with the simple atypical type. It developed in 29% of women with the complex atypical type.¹

A national Gynecologic Oncology Group study looked for cancer already present at the time of surgery. Each woman's biopsy showed the atypical type. All of them went straight to surgery to remove the uterus (hysterectomy).

In 42.6% of these women, the uterus already contained invasive cancer.² The biopsy had missed it.

The type without atypia carries a much lower cancer risk. It often resolves once hormone balance returns.

The root cause is a hormone imbalance. The common drivers are long stretches without ovulation, polyendocrine metabolic ovarian syndrome (PMOS / PCOS), obesity, estrogen taken without progesterone, and tumors that make estrogen.

Cycle charting finds anovulatory cycles and a disrupted luteal phase early. It finds them before the overgrowth sets in. The hormone problem shows on the chart before it shows on a biopsy.

Progesterone therapy reverses many cases without atypia. It balances the excess estrogen.³ Some women with the atypical type want to have children later. For them, high-dose progestin therapy is a recognized option before hysterectomy. It requires close checks of the lining.

In either type, the restorative principle is to address the source of excess estrogen, not only to treat the lining.