Progesterone is a steroid hormone primarily known for its role in the female reproductive system. Its main function is to prepare the lining of the uterus, the endometrium, for the potential implantation of a fertilized egg and to support early pregnancy. If conception does not occur, the drop in progesterone levels triggers the start of menstruation. A deficiency can disrupt the menstrual cycle, cause irregular bleeding, and lead to difficulties in conceiving or maintaining a pregnancy. Understanding the causes of this deficiency requires looking at both the direct failure of the hormone-producing organ and the systemic influences that interfere with its production.
Primary Causes Related to Ovarian Function
The most direct cause of progesterone deficiency stems from issues within the ovary. Progesterone is secreted by the corpus luteum, a temporary structure that forms from the ovarian follicle immediately after ovulation. Therefore, anything that prevents or compromises ovulation directly leads to low progesterone levels.
Anovulation, the failure to release an egg, is a common mechanism of deficiency. Since the corpus luteum never forms without ovulation, the necessary surge in progesterone during the second half of the cycle, known as the luteal phase, cannot occur. Conditions like Polycystic Ovary Syndrome (PCOS) or hypothalamic amenorrhea frequently cause anovulation by disrupting the complex hormonal signals that trigger egg release.
Even when ovulation does happen, Luteal Phase Defect (LPD) can still cause a deficiency. This defect means the corpus luteum that forms is either functionally inadequate, short-lived, or fails to produce sufficient progesterone to properly prepare the uterine lining. A short luteal phase, often defined as less than 10 days, results in a prematurely low progesterone level, which can prevent a fertilized egg from implanting or lead to early miscarriage.
Age-Related Hormonal Decline
Progesterone deficiency also occurs as a natural part of the aging process, particularly during the transition to menopause. This decline is directly linked to the decrease in ovarian reserve. As a woman enters perimenopause, ovulatory cycles become less consistent and anovulatory cycles become more frequent.
Since progesterone is produced only after ovulation, the increasing frequency of cycles without an egg release causes a significant, sometimes erratic, drop in overall progesterone production. This decline often begins earlier and is more precipitous than the drop in estrogen levels, a phenomenon that can lead to symptoms often described as “estrogen dominance.” The relative imbalance between the two hormones, rather than high estrogen alone, drives many perimenopausal symptoms.
Once a woman reaches menopause, the ovaries have effectively ceased functioning. The primary source of progesterone is lost because ovulation and the formation of the corpus luteum are no longer occurring. Progesterone levels remain chronically low, typically falling to 0.20 ng/mL or less, which is characteristic of the postmenopausal state.
Systemic Factors and Endocrine Influences
Progesterone production is influenced by external factors and other endocrine organs. Chronic, unmanaged stress is a significant systemic factor that can interfere with hormone balance. The body prioritizes the production of the stress hormone cortisol, especially under prolonged duress.
This prioritization is sometimes referred to as the “pregnenolone steal” or “hormone steal” effect, where the shared precursor molecule, pregnenolone, is diverted away from the synthesis pathway for progesterone toward making cortisol, resulting in a reduced pool of material available for progesterone synthesis. The chronic elevation of cortisol also suppresses the hypothalamic-pituitary-ovarian (HPO) axis, which is the command center for the reproductive cycle.
Dysfunction in the thyroid gland, particularly hypothyroidism, is another indirect cause. Low levels of thyroid hormone can disrupt the HPO axis, leading to irregular cycles and anovulation. This systemic disruption prevents the proper development of the follicle and the subsequent formation of the corpus luteum, thereby causing a progesterone deficiency.
Rapid weight changes, extreme dieting, and excessive exercise can also trigger progesterone deficiency through the central nervous system. These activities can signal a state of energy deficit to the hypothalamus, suppressing the release of the hormones needed to initiate ovulation. This hypothalamic dysfunction results in anovulation, preventing the production of progesterone. Lastly, a relative deficiency can be created by high estrogen levels, which do not directly reduce progesterone but can suppress the pituitary hormones required for its production, creating an imbalanced state often called estrogen dominance.