In 1949, Georgeanna Jones, MD, first described luteal phase deficiency (LPD).  The inadequate secretory transformation of the endometrium, resulting from deficient progesterone production, has been implicated in both infertility and recurrent pregnancy loss. [2, 3] LPD has been the subject of much debate among specialists in the field of reproductive endocrinology since Jones' introduction of this condition into the medical literature. LPD has been diagnosed in 3-20% of patients who are infertile and in 5-60% of patients experiencing recurrent pregnancy loss. However, data show that 6-10% of women who are fertile demonstrate an inadequate luteal phase, which confirms the need for a better understanding of normal variations in the menstrual cycle and in variations that could be pathologic.
This article addresses healthy menstrual physiology, the proposed pathophysiology of LPD, current methods available for diagnosis and treatment, and reasons for the controversy surrounding this subject.
Healthy menstrual physiology
Following ovulation, the mature ovarian follicle forms the corpus luteum, which becomes a blood-filled structure that allows the precursor cholesterol to be obtained, initiating steroidogenesis and resulting in progesterone production. Whereas the follicular phase of the menstrual cycle can vary in length, the secretory phase lasts approximately 14 days, correlating with the life span of the corpus luteum. Presumably, progesterone prepares the endometrium for implantation and maintenance of a pregnancy. If pregnancy occurs, the production of progesterone from the corpus luteum continues for 7 weeks because of the tonic release of luteinizing hormone (LH) from the pituitary gland. Studies show that after 7 weeks, the placenta takes over this function. If pregnancy does not occur, menses begins with the demise of the corpus luteum.
For related information, see Medscape's Pregnancy Resource Center.
The following mechanisms can cause an inadequate endometrial response to hormonal stimulation during the luteal phase. 
Abnormal follicular development
Abnormal follicular development results from inadequate follicle-stimulating hormone (FSH) and luteinizing hormone (LH) secretion from the anterior pituitary gland. FSH stimulates the granulosa cells of the developing follicle to produce estradiol from the conversion of its substrate androstenedione. A decrease in FSH release results in reduced granulosa cell growth and lower estradiol levels. Because the corpus luteum is not a de novo structure but is a direct result of the follicle, it shows the effects of abnormal folliculogenesis with decreased progesterone production.
An inadequate LH release can cause a decrease in androstenedione from the theca cells. Less substrate results in a decrease in estradiol and, subsequently, lower progesterone levels. Additionally, a suboptimal LH surge at ovulation causes deficient progesterone because of inadequate luteinization of the granulosa cells.
Uterine abnormalities cause changes in vascularization of the endometrium despite normal progesterone levels. Myomas, uterine septa, and endometritis are responsible for poor secretory changes in the endometrium.
Hypocholesterolemia is the substrate responsible for initiation of the steroid pathway. A deficiency results in low-to-absent progesterone production and a luteal phase defect.
No consensus has been achieved regarding frequency; however, a 1991 symposium hypothesized that luteal phase deficiency (LPD) occurs in 3-10% of infertile patients, and healthy women have deficient luteal phase production of progesterone on a sporadic basis.
Presumably, international frequency is similar to that in the United States.
No morbidity or mortality has been associated with this condition.
Luteal phase deficiency affects women of all races.
Luteal phase deficiency affects only women.
Luteal phase deficiency primarily affects women during their reproductive years.
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