Infertility :: New discovery may help doctors treat infertility

New research suggests that medications commonly referred to as fertility drugs may be ineffective for women who lack a gene called the estrogen receptor beta. The study showed that fertility drugs did not improve ovulation rates in mice that were genetically engineered to lack estrogen receptor beta. The estrogen receptor beta is one of two estrogen receptor proteins which mediate the effects of estrogen hormones and are present throughout the female reproductive tissues. These new data indicate that this receptor plays a critical role in ovulation, and suggests that women who do not have this receptor may benefit more from alternative infertility treatments. The findings are reported in Endocrinology.

“What we found is that the beta estrogen receptor plays a role in moving the egg outside the ovary so it can be fertilized,” said Kenneth Korach, Ph.D., Laboratory Chief at the National Institute of Environmental Health Sciences (NIEHS) where the research was conducted. “We never knew before what function this receptor played in reproduction.”

If the results from this animal study are found to be applicable to humans, a simple blood test will be able to provide enough information to determine if a genetic mutation may be altering the function of the estrogen receptor beta. The results of this blood test, coupled with information from other medical tests and evaluations conducted by the physician, will help diagnose infertility and better determine treatment options.

“Dealing with infertility can be emotionally, financially, and physically draining” said Dr. David Schwartz, Director of the NIEHS, a part of the National Institutes of Health, which funded the research. “If we can help couples understand the reasons for their infertility, doctors can further define their treatment options, help them to minimize the expense and risk of taking drugs that may be less effective for them, and increase their chances of having a safe and healthy child,” he added.