About Fertility
What is Luteal Phase Defect?
The proposal of a luteal phase defect (LPD) has floated around infertility forums and research for years. The data supporting its existence remains thin. What is a luteal phase defect? It is defined as “the condition where progesterone from corpus luteum is not sufficient to maintain endometrium and pregnancy.”
How Does a Luteal Phase Defect Affect Fertility?
There is a crosstalk between the blastocyst (the embryo ready for implantation), then endometrium, and the source of progesterone. The blastocyst, at day seven or eight (once implanted into the endometrium), will begin to produce minute amounts of HCG (pregnancy hormone). This hormone will help maintain the corpus luteum (the follicle that releases the egg). The corpus luteum provides progesterone, which, in turn, supports further the establishment and growth of the developing embryo.
Without the corpus luteum (and its progesterone), there is no pregnancy. Without the implanting embryo (and pregnancy), there is no maintained corpus luteum.
Can You Get Pregnant with a Short Luteal Phase?
A defective luteal phase—the absence of sufficient progesterone—and its effect on the detrimental effects of pregnancy is a thin veil. It is defined as a phase from ovulation to the period (the luteal phase) of less than nine days. Interestingly, less than 10% of fertile women have a luteal phase of the same length. Therefore the chronologic “shortening” of the luteal phase is not necessarily the harbinger of infertility. It has never been proven to be a cause of infertility.
How is a Luteal Phase Defect Diagnosed?
In fact, the ability to diagnose LPD remains equally elusive. Hormone levels, basal body temperatures, and/or endometrial biopsy all provide variable effects. Not only is it difficult to define, but it is also impossible to diagnose (even if it truly exists). Predictably, a condition difficult to define and diagnose is expected to be difficult to correct or treat.
Progesterone supplementation is suggested as a treatment for LPD, replenishing the source expected to be impaired. It is the mainstay of treatment, although there is no evidence that it improves pregnancy outcomes in natural cycles. It is provided in pill, vaginal cream, and injection form—to no avail and, most likely, no benefit other than to soothe the soul.
In patients with recurrent pregnancy loss, sometimes an ovulation induction agent, such as Clomid, is employed. The idea being that a “stronger” follicle would be more likely to support the progesterone production at the corpus luteum state. But there’s a lack of data here, too.
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