No form of contraception is 100 percent effective, and a fascinating new study has provided a possible explanation for why that is the case for one of the most widely used forms of birth control. The research has for the first time linked a specific genetic variant with the efficacy of hormone-based birth control treatments, suggesting this type of contraception may be less effective in women found with this particular gene.
The majority of current birth control drugs work by delivering certain hormones to a woman, preventing her ability to become pregnant. Failure rates for these contraceptives can vary but generally it is thought that when properly and consistently administered, hormonal birth control can be effective up to 99.7 percent of the time.
We don't know exactly why these contraceptives occasionally fail, and often when they do it is the user who is blamed for incorrectly taking the drug. Maybe a dose was skipped or taken slightly later than it should have been. New research is suggesting for the first time that it could be a specific genetic variant that is actually making birth control drugs less effective in some women.
"When a woman says she got pregnant while on birth control the assumption was always that it was somehow her fault," says Aaron Lazorwitz, from the University of Colorado School of Medicine and lead author on the new study. "But these findings show that we should listen to our patients and consider if there is something in their genes that caused this."
Pharmacogenomics is the study of how specific genes influence the effects of certain drugs. Study into how drug metabolism is affected by genetics has been around for some time but it is only recently that computational power and genomic data has progressed to the point that researchers can seriously investigate these connections.
The new research looked at 350 women using a contraceptive implant that releases etonogestrel, a progestin-based form of hormonal birth control, and focused on a number of genes that govern steroid hormone metabolism and function. One specific gene appeared to play a major role in enhancing the body's ability to metabolize etonogestrel.
Called CYP3A7*1C, this gene is primarily active in fetal development, producing a enzyme called CYP3A7 that alters steroid hormone metabolism. Although it is generally switched off at birth, the research found the gene still remained active in five percent of the women studied. Over one quarter of the women with this gene still active were found to have etonogestrel levels below the recommended limit needed to achieve consistent ovulatory suppression.
"That enzyme breaks down the hormones in birth control and may put women at a higher risk of pregnancy while using contraceptives, especially lower dose methods," says Lazorwitz.
It is worth noting that this study should not raise concerns for women on birth control as these treatments are still incredibly effective when used correctly. The research does however highlight the importance in understanding how a person's unique genetic fingerprint can profoundly influence their ability to metabolize certain drugs.
It is still early days for this kind of research, and pharmacogenomic tests are not widely available, but Lazorwitz does suggest this kind of personalized medicine, underpinned by genomic analysis, will be important in the future, particularly in the realm of women's reproductive health.
"As more genetic data becomes available, clinicians may need to consider adding genetic predisposition to increased steroid hormone metabolism in their differential diagnosis for unintended pregnancies in women reporting perfect adherence to hormonal contraceptive methods," Lazorwitz concludes.
The new research was published in the journal Obstetrics & Gynecology.
Want a cleaner, faster loading and ad free reading experience?
Try New Atlas Plus. Learn more