Ovulation is the central event of the menstrual cycle, representing the release of a mature egg from the ovary. This process is orchestrated by a complex feedback system involving the brain and the ovaries. When this hormonal sequence is disrupted, the egg fails to mature and release (anovulation), or it happens infrequently (oligoovulation). A chronic pattern of infrequent or absent ovulation is often the primary reason for irregular periods and can signal an underlying health issue.
Lifestyle and Environmental Triggers
The body’s reproductive system is highly sensitive to external inputs, particularly energy balance and stress perception. Significant changes in weight, either rapid gain or loss, can interfere with the signals needed to initiate ovulation. Low body fat causes the hormone leptin to drop, suppressing the pulsatile release of Gonadotropin-Releasing Hormone (GnRH) from the hypothalamus. Conversely, excessive body fat increases peripheral hormone conversion, resulting in elevated estrogen that suppresses the follicular phase hormones required for egg maturation.
Chronic psychological or physical stress also directly impacts the reproductive axis by triggering the Hypothalamic-Pituitary-Adrenal (HPA) axis. This stress response increases cortisol production, which suppresses the GnRH pulse generator in the brain. The resulting decrease in Luteinizing Hormone (LH) and Follicle-Stimulating Hormone (FSH) diverts energy away from reproduction. This functional disruption is often temporary and can be reversed through diet, exercise, and stress management. Anovulation is also common immediately following the discontinuation of hormonal birth control. It can take several months for the body’s natural hormonal feedback loop, suppressed by synthetic hormones, to fully re-establish a regular ovulatory pattern.
Systemic Hormonal Conditions
Chronic endocrine diseases can prevent the ovaries from releasing an egg. Polycystic Ovary Syndrome (PCOS) is the most common cause of chronic anovulation, affecting up to one in ten women of reproductive age. The core issue in PCOS is an accelerated pulsatile secretion of GnRH, which favors the production of LH over FSH from the pituitary gland. This creates a characteristic high LH-to-FSH ratio, often considered greater than two-to-one.
Excessive LH stimulation causes ovarian theca cells to overproduce androgens, such as testosterone. This high androgen level, combined with insufficient FSH, causes developing follicles to stall at a small size (typically two to eight millimeters). These arrested follicles accumulate in the ovary, creating the polycystic appearance. Their failure to mature results in the absence of a dominant follicle and no ovulation. Insulin resistance, a common feature in PCOS, further enhances ovarian androgen production.
Disorders of the thyroid gland frequently disrupt ovulation due to the interconnectedness of endocrine systems. In hypothyroidism, low thyroid hormone levels increase the production of Thyrotropin-Releasing Hormone (TRH). TRH stimulates both Thyroid-Stimulating Hormone (TSH) and prolactin release. Elevated prolactin levels (hyperprolactinemia) are a direct cause of ovulatory dysfunction. Excess prolactin actively inhibits the pulsatile release of GnRH from the hypothalamus. This suppression of GnRH leads to lower levels of LH and FSH, preventing the ovary from preparing and releasing a mature egg.
Primary Ovarian Concerns
Sometimes, the issue lies not with systemic hormonal signaling from the brain, but with the ovarian reserve itself. Primary Ovarian Insufficiency (POI) is a condition where the ovaries cease to function normally before age 40 due to premature depletion or dysfunction of the follicles. POI is marked by a hormonal profile opposite to many other anovulatory disorders. As follicles fail, the ovary produces less estrogen, leading to a loss of negative feedback to the pituitary. This results in significantly elevated levels of FSH and LH as the brain attempts to stimulate the non-responsive ovaries.
The transition into perimenopause, the years leading up to menopause, also causes increasingly erratic ovulation patterns. As the pool of available follicles dwindles with age, the production of Inhibin B decreases. Inhibin B normally helps regulate FSH; its decline causes FSH levels to become highly variable and often elevated. This hormonal fluctuation leads to cycles that can be shorter or much longer than normal, with anovulation becoming more frequent as the ovaries struggle to respond effectively.
Seeking Diagnosis and Management
A medical evaluation is recommended if menstrual cycles are consistently irregular (shorter than 21 days or longer than 35 days), or if periods have been absent for 90 days. The diagnostic process begins with blood tests to map the hormonal environment. Key tests include a mid-luteal phase progesterone level, typically drawn seven days before the expected period, to confirm if ovulation occurred.
Early follicular phase blood work, often drawn on cycle day three, measures FSH and LH to check ovarian reserve and for the LH/FSH imbalance seen in PCOS. TSH and prolactin levels are checked to rule out thyroid and hyperprolactinemia causes. Androgen levels confirm the presence of excessive male hormones. Imaging, such as a pelvic or transvaginal ultrasound, visualizes the ovaries, looking for the ring of small follicles associated with PCOS or the small, quiet ovaries indicative of POI. Management focuses on addressing the root cause through targeted lifestyle modifications, medications, or ovulation-inducing therapies.