Emanuela Lazzaroni-Tealdi, MS, is a reproductive biologist and senior embryologist with nearly 20 years of experience in assisted reproduction. Throughout her career, she has worked with some of the most renowned fertility centers in the United States, including NYU Langone, Northwell Health, and the Center for Human Reproduction. Emanuela brings deep scientific expertise and a patient-centered approach to every aspect of fertility care, with a special interest in IVF and the impact of endometriosis on reproductive health. At ESSI, she is in charge of the Peer Support Program and medical education.
Q: Can you start by explaining how endometriosis can interfere with fertility?
A: Endometriosis can interfere with fertility on several levels. Anatomically, it may cause adhesions or distort pelvic structures, affecting the ovaries, fallopian tubes, and uterus. But even in the absence of visible distortion, the disease creates a pro-inflammatory environment in the pelvis, full of cytokines, oxidative stress, and immune cells, which can damage the quality of the egg and the viability of sperm. This hostile environment can also impair fertilization and embryo development, even during IVF.
Q: Is there evidence that endometriosis affects egg quality directly?
A: Yes, and it’s becoming increasingly clear. Studies have shown that women with endometriosis tend to have lower-quality oocytes, reduced mitochondrial function, and impaired fertilization and blastocyst development rates. A 2020 meta-analysis published in Reproductive Biomedicine Online confirmed poorer embryo quality and reduced cumulative live birth rates in women with endometriosis, even when using IVF. Chronic inflammation and oxidative stress are key players here, compromising the delicate microenvironment needed for healthy oocyte maturation.
Q: What about adenomyosis? How does it affect fertility?
A: Adenomyosis is another complex player in fertility. It involves the presence of endometrial tissue within the uterine muscle wall, which causes chronic inflammation, altered uterine contractility, abnormal angiogenesis, and progesterone resistance. These changes disrupt the endometrial receptivity necessary for implantation. As a result, women with adenomyosis often face lower implantation rates and higher miscarriage rates, even in IVF cycles. One notable study in Human Reproduction Update (2017) emphasized how adenomyosis alters the function of the endometrial-myometrial interface, which is critical for early embryo attachment.
Q: Let’s talk about immune dysfunction. How does it contribute to implantation failure and miscarriage in endometriosis patients?
A: This is such an important area that is often overlooked. Endometriosis is not just a mechanical disease; it’s an immune and inflammatory condition. Women with endometriosis often show dysregulation of immune cells, especially uterine natural killer (uNK) cells, macrophages, and T-regulatory cells, which are critical for establishing tolerance to the embryo.
In cases of recurrent implantation failure (RIF) and recurrent pregnancy loss (RPL), research shows increased activation of cytotoxic NK cells, elevated pro-inflammatory cytokines (like TNF-α, IL-1β), and impaired immune tolerance at the maternal-fetal interface. Essentially, the immune system may fail to properly recognize and support the embryo, contributing to implantation failure or early pregnancy loss. This is particularly true in patients with both endometriosis and adenomyosis.
In my professional experience, I’ve seen many patients benefit from immune testing and modulation, especially when traditional IVF fails repeatedly. Treatments may include immunosuppressive therapies like prednisone, IVIG, intralipids, or anticoagulants, although they remain controversial and require careful patient selection.
Q: Are IVF outcomes different for patients with endometriosis and adenomyosis?
A: Yes. IVF outcomes are often lower in women with moderate to severe endometriosis and those with adenomyosis. The disease can lower oocyte yield, affect embryo quality, and reduce implantation and live birth rates. However, outcomes vary significantly based on age, ovarian reserve, and treatment protocols.
Q: How do you counsel patients struggling with endometriosis, adenomyosis, and infertility?
A: I always start by saying this: You are not alone, and your pain is real. Then, I try to empower each patient with knowledge. Endometriosis and adenomyosis are complex, and so is fertility. However, understanding how these conditions work biologically, hormonally, and immunologically can help patients make informed decisions.
Sometimes IVF is the answer. Sometimes it’s surgery first. Sometimes it’s a combination. And increasingly, we are learning that addressing immune dysregulation is a missing piece of the puzzle. My goal is to offer scientific expertise and compassionate, personalized guidance because that’s what patients with endometriosis truly need.
