Why Is My Endometrium Thin and What Causes It?

The endometrium, or uterine lining, is a specialized tissue inside the uterus. Its primary function is to prepare for the implantation of a fertilized egg, serving as the receptive site for pregnancy. If conception does not occur, the top layer of the endometrium is shed during menstruation. While thickness variations are normal during the cycle, a chronically thin lining can raise concerns about menstrual health or fertility. This persistent thinness is defined as a measurement below a specific threshold, requiring investigation into its causes.

Understanding the Endometrium and Normal Thickness

The endometrium is a dynamic tissue responding to fluctuating reproductive hormones throughout the menstrual cycle. During the proliferative phase (the first half of the cycle), estrogen stimulates the lining to rebuild and thicken after menstruation. This growth creates a vascular and nutrient-rich environment essential for a potential embryo.

A “thin” endometrium is clinically defined as a thickness of less than 7 millimeters (mm) during the late proliferative phase, just before ovulation. Normal thickness varies significantly, starting at 2 to 4 mm during menstruation and ideally reaching 8 mm to 16 mm around ovulation. A measurement consistently below the 7 mm threshold is associated with decreased rates of successful embryo implantation and a higher risk of early pregnancy loss.

Primary Causes of Thin Endometrium

A consistently thin endometrial lining stems from hormonal imbalance, structural damage, or medication side effects. The most common cause is inadequate stimulation from estrogen, the hormone responsible for tissue growth and proliferation. Low estrogen levels, resulting from age, ovarian dysfunction, or endocrine disorders, fail to prompt necessary cellular growth and blood vessel development.

Structural damage to the uterus is another cause, most notably Asherman’s Syndrome (AS), which involves the formation of intrauterine adhesions or scar tissue. This scarring often develops after surgical procedures, such as aggressive dilation and curettage (D&C) following miscarriage or childbirth, or severe pelvic infections. The scar tissue prevents the basal layer of the endometrium, which contains stem cells for regeneration, from properly regrowing the functional layer each month.

Certain medications can also directly inhibit the growth of the uterine lining, even when hormone levels are normal. Clomiphene Citrate (Clomid), a common oral fertility medication, sometimes blocks estrogen receptors in the endometrium. By acting as an anti-estrogen, this medication suppresses the lining’s proliferative response, leading to a thinner measurement.

The physical supply of blood to the uterus, known as uterine perfusion, is also a factor. Poor blood flow impedes the delivery of oxygen, nutrients, and hormones necessary for the lining’s rapid growth. Vascular issues may arise from structural problems, chronic inflammation, or specific circulatory conditions, contributing to a non-responsive endometrium.

How Thin Endometrium is Diagnosed

Diagnosis of a thin endometrium typically begins with the patient reporting symptoms like unusually light or short menstrual periods, or recurrent implantation failure in fertility treatment. The primary diagnostic tool is the transvaginal ultrasound, which allows a clear and non-invasive measurement of the endometrial thickness. This measurement is ideally taken during the mid-proliferative phase of the cycle, when the lining should be nearing its peak thickness.

If a thin lining is confirmed, further investigation is needed to determine the underlying cause. Blood tests are performed to assess hormonal status, focusing on levels of Estradiol, the main form of estrogen responsible for endometrial proliferation. A specialized ultrasound called Saline Sonohysterography (SIS) may be used to inflate the uterine cavity with saline solution, providing a clearer view of the lining’s contour and identifying potential structural abnormalities.

For cases suspected to involve scar tissue, hysteroscopy is often the most definitive diagnostic procedure. This minimally invasive technique involves inserting a small camera through the cervix to directly visualize the uterine cavity. Hysteroscopy confirms the presence, location, and severity of intrauterine adhesions, the hallmark of Asherman’s Syndrome.

Strategies for Increasing Endometrial Thickness

Treatment for a thin endometrium is tailored to address the specific underlying cause identified during diagnosis. For hormonal deficiencies, the most common medical strategy involves supplemental estrogen therapy. Estrogen can be administered orally, via transdermal patches, or vaginally, with the goal of directly stimulating the proliferation of endometrial cells.

When poor blood flow is suspected, therapies focused on increasing uterine perfusion may be recommended. These supportive treatments often include vasoactive substances like low-dose aspirin, which improves circulation, and L-arginine, an amino acid that aids in producing nitric oxide (a strong vasodilator). Vitamin E is sometimes used as an antioxidant to support improved circulation to the pelvic organs.

If the thinness is caused by structural damage like Asherman’s Syndrome, surgical intervention is necessary to restore the uterine cavity. This involves a hysteroscopic lysis of adhesions, where the scar tissue is carefully cut and removed using specialized instruments guided by the camera. Following surgery, high-dose estrogen therapy is typically used to promote the regrowth of a healthy lining and prevent the recurrence of scarring.

In cases where a fertility drug like Clomiphene Citrate is the culprit, treatment involves switching to a different ovulation-inducing medication or adding supplemental estrogen to counteract the drug’s anti-estrogen effects. Newer options, such as Platelet-Rich Plasma (PRP) infusion, which delivers growth factors directly to the lining, are also being explored when the endometrium does not respond to traditional hormonal treatment. Working closely with a reproductive specialist helps determine the most appropriate path forward.