I Haven’t Had My Period in 3 Months but Pregnancy Tests Are Negative

The absence of a menstrual period for three or more consecutive cycles is medically termed secondary amenorrhea. When pregnancy tests are negative, this signals a disruption in the complex hormonal signaling that governs the reproductive system. The cessation of the menstrual cycle suggests the body is responding to an underlying imbalance or diverting resources. Seeking professional evaluation is appropriate to identify the specific cause and prevent potential long-term health consequences.

Lifestyle Factors Disrupting the Cycle

The body’s reproductive function is highly sensitive to external stressors, often causing functional hypothalamic amenorrhea (FHA). This occurs when the hypothalamus, the brain region regulating hormone production, suppresses the signals necessary for ovulation. Significant changes in body weight, including being underweight or experiencing substantial weight loss, can trigger this mechanism.

An energy deficit caused by excessive, high-intensity physical activity without sufficient caloric intake can also halt the cycle. Endurance training combined with dietary restriction signals to the body that it is not safe to support a pregnancy. This hormonal suppression leads to a temporary hypoestrogenic environment.

Chronic psychological or emotional stress activates the hypothalamic-pituitary-adrenal (HPA) axis. This increases the release of stress hormones, which interferes with the pulsatile secretion of gonadotropin-releasing hormone (GnRH). When the GnRH pulse generator slows down, the downstream hormones required for ovulation—Follicle-Stimulating Hormone (FSH) and Luteinizing Hormone (LH)—are not adequately released, and the menstrual cycle stops.

Hormonal and Endocrine Imbalances

Internal medical conditions originating in the endocrine system can also stop the menstrual cycle. Polycystic Ovary Syndrome (PCOS) is a frequent endocrine cause of secondary amenorrhea, characterized by anovulation and hyperandrogenism. Insulin resistance often drives the ovaries to produce excess androgens, such as testosterone.

This excess androgen disrupts the normal feedback loop, causing a persistently elevated LH level relative to FSH. This imbalance prevents ovarian follicles from maturing and releasing an egg, leading to chronic anovulation. Ovaries may develop a characteristic appearance on ultrasound due to many small, arrested follicles.

Dysfunction of the thyroid gland significantly impacts the reproductive axis. An underactive thyroid (hypothyroidism) can increase Thyrotropin-Releasing Hormone (TRH) production. High TRH levels stimulate the pituitary gland to release excess prolactin, causing hormonal disruption.

Conversely, an overactive thyroid (hyperthyroidism) can increase Sex Hormone Binding Globulin (SHBG), which binds to reproductive hormones and alters their availability. Both hypo- and hyperthyroidism interfere with the pituitary’s regulation of FSH and LH, preventing the hormonal surge needed for ovulation. Treating the underlying thyroid disorder often restores the regular menstrual cycle.

Hyperprolactinemia, an elevated level of prolactin, is another cause. Excess prolactin inhibits the normal pulsatile release of GnRH from the hypothalamus. This suppression leads to insufficient levels of FSH and LH, effectively shutting down ovarian function and causing anovulation.

Hyperprolactinemia can be caused by a benign tumor on the pituitary gland (prolactinoma) or by certain medications. Less commonly, Premature Ovarian Insufficiency (POI), defined as the loss of normal ovarian function before age 40, can be the underlying cause. In POI, the ovaries fail, resulting in low estrogen and a compensatory high level of FSH and LH, as the pituitary attempts to stimulate the non-responsive ovaries.

Medications and Recent Contraceptive Changes

Various medications can directly or indirectly suppress the menstrual cycle. Recently discontinuing hormonal birth control can result in a temporary delay in the return of natural cycles, known as post-pill amenorrhea. Although synthetic hormones leave the body quickly, the hypothalamic-pituitary-ovarian axis needs time to resume its own regulation.

This delay usually resolves within three to six months, but it may unmask a pre-existing condition, such as PCOS, that the pill was managing. Certain long-acting hormonal contraceptives, like the Depo-Provera injection, are designed to cause amenorrhea. The continuous progestin suppresses ovulation and causes the uterine lining to become thin, eliminating monthly bleeding.

Other medications, particularly antipsychotics and some antidepressants, can cause amenorrhea as a side effect. These drugs often affect dopamine, which naturally suppresses prolactin release. By blocking dopamine receptors, these medications can induce hyperprolactinemia, suppressing the GnRH pulse generator and halting the menstrual cycle.

Diagnostic Steps and When to See a Doctor

The absence of a period for three months warrants a medical appointment, even with a negative home pregnancy test. A healthcare provider will begin with a thorough review of medical history, including recent changes in weight, exercise, stress levels, and medications. A physical examination will check for signs of hormonal imbalance, such as excess body hair, acne, or a milky discharge from the nipples.

The initial workup involves targeted blood tests to identify the hormonal disruption. These include measuring TSH (Thyroid-Stimulating Hormone) and prolactin levels to rule out thyroid dysfunction and hyperprolactinemia. Gonadotropin levels (FSH and LH) are also measured to locate the source of the problem.

High FSH and LH levels point toward an ovarian issue like POI, while low or normal levels suggest a problem in the hypothalamus or pituitary, such as FHA. If symptoms suggest excess androgens, additional tests for testosterone and other androgen levels will be ordered to confirm or rule out PCOS. A pelvic ultrasound may be performed to visualize the ovaries for polycystic morphology and to assess the thickness of the uterine lining, which reflects estrogen exposure.