Dehydroepiandrosterone (DHEA) is a naturally occurring steroid hormone produced mainly by the adrenal glands and, to a lesser extent, the ovaries. As a precursor to sex hormones like testosterone and estrogen, DHEA plays a vital role in reproductive health. Recent research, particularly by Dr. Norbert Gleicher and his team at the Center for Human Reproduction (CHR) in New York, highlights DHEA’s potential to enhance ovarian reserve in women with diminished ovarian reserve (DOR) or premature ovarian aging (POA). This blog explores why and how DHEA can improve ovarian reserve, drawing on Gleicher’s groundbreaking data.
What Is Ovarian Reserve?
Ovarian reserve refers to the quantity and quality of a woman’s remaining eggs, which naturally decline with age or due to conditions like DOR or POA. Women with DOR often face challenges in achieving pregnancy, as they have fewer eggs and may produce lower-quality embryos during in vitro fertilization (IVF). Dr. Gleicher’s research focuses on improving fertility outcomes for these women, particularly those over 40 or with premature ovarian aging, by leveraging DHEA supplementation.
Why DHEA? The Benefits for Ovarian Reserve
DHEA is a promising tool for enhancing ovarian reserve because it supports the production of androgens, such as testosterone, which are essential for early follicle development in the ovaries. Women with DOR often have low androgen levels, which can hinder follicle growth and lead to poor egg quality. By supplementing with DHEA, women can optimize their ovarian environment, improving both the quantity and quality of eggs. According to Dr. Gleicher’s studies, DHEA offers several key benefits:
- Increased egg and embryo yields: DHEA supplementation boosts the number of oocytes retrieved and embryos produced during IVF cycles.
- Improved egg and embryo quality: DHEA enhances the chromosomal integrity of embryos, increasing the chances of successful pregnancies.
- Higher pregnancy rates: Women using DHEA show improved clinical pregnancy rates in IVF.
- Reduced miscarriage rates: By improving embryo quality, DHEA lowers the risk of pregnancy loss.
How DHEA Enhances Ovarian Reserve
Dr. Gleicher’s research outlines several mechanisms by which DHEA improves ovarian function:
- Supporting Folliculogenesis with Androgens: DHEA is converted into testosterone in the ovaries, which interacts with androgen receptors on granulosa cells. This synergy with follicle-stimulating hormone (FSH) promotes early follicle development up to the pre-antral stage, enhancing functional ovarian reserve (FOR). Gleicher’s studies show that this process is reflected in increased anti-Müllerian hormone (AMH) levels, a key marker of ovarian reserve.
- Improving Embryo Quality: A 2010 study by Gleicher using preimplantation genetic screening (PGS) demonstrated that DHEA supplementation (75 mg/day) significantly reduced the number of aneuploid embryos (2.8 ± 2.5 in DHEA patients vs. 4.5 ± 3.1 in controls; P = 0.03), indicating better egg and embryo quality.
- Boosting AMH Levels: In a 2009 study, Gleicher found that women with DOR who took 75 mg of DHEA daily (25 mg three times daily) for 30–120 days showed significant increases in AMH levels (P = 0.002), particularly in younger women with POA, suggesting improved ovarian reserve.
- Enhancing IVF Outcomes: A 2006 case-control study by Gleicher and Barad reported that DHEA supplementation led to significant increases in fertilized oocytes (P < 0.001), normal day-3 embryos (P = 0.001), and embryos transferred (P = 0.005) during IVF cycles, improving overall fertility outcomes.
These findings suggest that DHEA acts as a “rejuvenating” agent for the ovaries, particularly in women with low androgen levels due to adrenal insufficiency. By optimizing the ovarian environment, DHEA supports healthier follicle development and better reproductive outcomes.
Key Findings from Dr. Norbert Gleicher’s Research
Dr. Gleicher’s pioneering work at CHR provides robust evidence for DHEA’s role in fertility:
- 2006 Study (Human Reproduction): In a case-control study of 25 women with DOR, 75 mg/day of DHEA for approximately 17.6 weeks significantly improved oocyte yields, embryo quality, and transfer rates compared to pre-DHEA IVF cycles.
- 2009 Study (Fertility and Sterility): A cohort study of 120 women with DOR showed that DHEA supplementation increased AMH levels, with younger women experiencing the most significant improvements, leading to higher cumulative pregnancy rates.
- 2009 Miscarriage Study (Reproductive Biology and Endocrinology): In 73 DHEA-supplemented pregnancies, miscarriage rates were notably low (15.1% vs. national IVF averages; Mantel-Hänszel odds ratio 0.49, P = 0.04), particularly in women over 35.
- 2010 PGS Study (Reproductive Biology and Endocrinology): DHEA supplementation reduced aneuploidy in embryos, supporting its role in improving egg quality.
- 2011 Systematic Review (Reproductive Biology and Endocrinology): Analyzing 114 publications from 1995–2010, Gleicher concluded that DHEA enhances ovarian function, increases pregnancy rates, and reduces miscarriage risks, making it a valuable tool for women with DOR.
Who Can Benefit from DHEA?
DHEA supplementation is particularly effective for:
- Women with DOR or POA, especially those with low DHEA-S or testosterone levels.
- Women over 40 undergoing IVF, where ovarian reserve naturally declines.
- Patients with adrenal insufficiency contributing to low androgen levels.
A typical dose is 75 mg/day (25 mg three times daily), adjusted based on monthly blood tests.
Conclusion
DHEA supplementation, backed by Dr. Norbert Gleicher’s extensive research, offers a promising approach for women with diminished ovarian reserve seeking to improve their fertility outcomes. By supporting folliculogenesis, increasing AMH levels, improving embryo quality, and boosting pregnancy rates, DHEA has become a cornerstone of fertility treatment for many patients.
With DHEA, many women are finding renewed hope on their fertility journey.
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References
- Gleicher N, Barad DH. Reprod Biol Endocrinol. 2011;9:67.
- Gleicher N, et al. Reprod Biol Endocrinol. 2009;7:108.
- Barad D, Gleicher N. Hum Reprod. 2006;21:2845-2849.
- Gleicher N, et al. Fertil Steril. 2009;92:S54-S55.
- Gleicher N, et al. Reprod Biol Endocrinol. 2010;8:131.
