For thousands of years, severe pelvic pain was brushed off as something women were supposed to endure. Mothers told daughters it was normal — teachers said it was part of growing up. Even doctors were trained to believe it was just how female bodies worked. But what if the lining was never the same to begin with?

Inside the uterus is a layer called the endometrium. This lining thickens each month. If pregnancy does not happen, it sheds. That shedding is a “period”. It is predictable. It responds to hormones in a pattern.

That is normal endometrium. Now for the mind blowing part. Endometriosis is not that, and we are seeing new things with adenomyosis too.

Generations upon generations were told endometriosis was just bits of that lining that traveled backward during menstruation and implanted in the pelvis. That theory shaped medicine for over a century. It sounded simple — it was easy to repeat.

But it never explained everything. It did not explain why endometriosis has been found in young girls before their first period, in fetuses animals or even cases of cis men. It did not explain why lesions show up on the bowel, the diaphragm, or wrapped around nerves. It did not explain why the tissue behaves differently at a biological level.

Endometriosis lesions are not misplaced lining. They are abnormal cells that create lesions that produce their own estrogen. They often resist progesterone. They trigger ongoing inflammation. They grow new nerve fibers. They create pain that does not follow the rhythm of an external cycle — while self stimulating it’s own internal process.

They do not shed and disappear each month. Much of the misunderstanding around endometriosis comes from the idea that it behaves like that normal endometrium but outside the uterus. That it sheds, bleeds, and somehow redistributes through processes like retrograde menstruation. But that is not what we are seeing.

Endometriotic lesions are not simply pieces of lining that detach and relocate. They are biologically active tissue — they grow, invade, and sustain themselves in ways that normal endometrium does not. While bleeding can occur within or around these lesions, it is not the result of a coordinated shedding process. It is more often tied to inflammation, vascular changes, organ/tissue damage and the fragile, reactive nature of the tissue itself.

In some cases, lesions can appear blister-like, cystic, or deeply infiltrative. They can be clear, red, black, or fibrotic. They may spread across surfaces, wrap around structures, or burrow into tissue. These variations are not cosmetic differences. They reflect different biological behaviors.

What may look, at a glance, like “internal bleeding from a period” is not the same process at all. That misunderstanding has shaped decades of oversimplified explanations. That is why calling endometriosis a painful period is not just inaccurate — it is harmful.

Adenomyosis is also different in it’s own way, but it has been tangled into the same confusion. Adenomyosis happens when tissue similar to the inner lining grows into the muscle wall of the uterus. The muscle becomes thick and inflamed. The uterus can enlarge. Bleeding can become heavy. Cramps can become unbearable.

Under a microscope, adenomyosis and endometriosis can both show certain glands and supportive tissue called stroma. Normal endometrium also has glands and stroma. That overlap shaped decades of thinking.

But similar does not mean identical. More importantly, that was never the full picture.

More Than Glands and Stroma

For years, these glands and stroma were treated as the defining features of these diseases. They became the main course of how we understood them. Everything else was secondary or even non-existent. We are now beginning to understand that those features were only the starting point.

Beyond those structures is an entire biological environment that changes how both of these diseases behave — hormone signaling shifts, local estrogen production increases, progesterone resistance develops. The immune system responds differently. Inflammation becomes chronic. Nerve fibers grow where they should not and blood vessels reorganize. The tissue remodels itself. These are not supporting details — they are what define the disease itself.

Adenomyosis, in particular, reshapes the muscle of the uterus. The myometrium becomes reactive — it thickens. It changes how the uterus contracts and how blood flows through it. That environment is not passive. It is active and constantly influencing what happens inside the uterus.

Endometriosis behaves differently. It survives outside the uterus in environments where just don’t make sense. It sustains itself. It signals independently. It interacts with surrounding organs, nerves, and immune pathways in ways that normal endometrium does not.

So while these conditions may look similar in structure, they begin to separate in behavior. When we build entire frameworks of care based on what looks similar under a microscope, we risk missing everything happening beyond it.

For years, we focused on what was visible and overlooked the rest of the system. But the rest of the system is where the impact sits.

Why We Confused Them in the First Place

The confusion around these diseases was not random. It was built into how they were defined.

When the defining features are reduced to those microscopic glands and stroma, it becomes easy to group conditions together. It becomes easy to assume they share the same origin. It becomes easy to treat them as variations of the same process. That assumption shaped everything that followed and has been where we sat for quit literally 100 years — stand still research, diagnostics, and treatment. It delayed deeper understanding.

Adenomyosis could only be definitively diagnosed after hysterectomy for most of it’s time. That meant most research came from later-stage disease. We were studying what the condition looked like at the end, not how it developed over time. Now, with advances in imaging and emerging approaches to tissue sampling, we are beginning to see these diseases earlier and more clearly.

That shift is significant here. When we can study disease before organ removal, we can begin to understand its progression — not just its outcome. It also forces us to re-examine treatments built on incomplete understanding.

Procedures like uterine ablation target the inner lining of the uterus — but adenomyosis exists within the muscle. Treating the surface does not resolve what lies beneath it. In some cases, it can complicate diagnosis or leave the underlying disease unchanged. Same goes for ablation of endometriosis outside of the uterus.

When we only treat what is visible, we risk missing what is driving the condition. Better tools bring better clarity, clarity changes care.

Even the Definition Isn’t Settled

What becomes clear in current research is that the confusion is not just historically ongoing. There is still no universally accepted classification system for adenomyosis alone — not in imaging, not in pathology, not in how severity or subtypes are defined. Classification is not just academic. It determines how disease is recognized, how it is studied, and how treatment decisions are made.

This is part of why newer frameworks are beginning to shift the conversation. The AGE Classification System proposes separating adenomyosis, genital endometriosis, and extragenital disease into distinct but connected components, emphasizing anatomical involvement, disease burden, and surgical complexity. Rather than forcing these conditions into a single simplified category, it reflects something patients have long experienced — that these diseases do not follow one pattern. When classification begins to match biological reality, it changes how we stage disease, how we plan treatment, and how we measure outcomes.

Only more recently have imaging tools like ultrasound and MRI allowed clinicians to identify adenomyosis without removing the uterus. That shift has expanded visibility, but it has also exposed variability. Not just in how the disease presents, but in how it is interpreted. There is also no single agreed standard for how adenomyosis should appear on imaging either. Findings overlap. Criteria differ. What one provider identifies, another may miss.

What is seen does not always match what is felt — some patients with extensive disease may have minimal symptoms. Others with less visible findings experience severe pain, bleeding, and disruption to daily life. That disconnect reflects something patients have been saying for decades. Severity cannot be measured by appearance alone.

There are also emerging distinctions within adenomyosis itself. Some researchers describe internal forms affecting the inner uterine layers, and external forms located closer to the outer wall, sometimes overlapping with endometriosis. This is not just structural. It raises deeper questions about how these diseases overlap and how they are treated.

Even here, the origin is debated. Does the disease begin within the uterus and move outward overtime? Does it arise from processes outside the uterus and move inward, blurring the boundary even more? These are not minor differences in theory. They shape how we interpret imaging, how we classify disease and how we approach treatment. If internal and external forms develop through different mechanisms, then grouping them under a single label may overlook important biological differences.

This may also may help explain why some patients present with overlapping features of both conditions, and why separating them clinically is not always straight forward. What appears as two diagnoses may — in some cases — reflect a shared or interacting processes. But processes that differ from the native endometrium.

The answer is not settled. That uncertainty is not weakness in the field, just a signal that we are finally asking more precise questions. We are not working from finished definitions. We are working from moving ones and only now beginning to build systems capable of keeping up.

Which means the patients who have lived with this disease were never the outliers, they were the evidence. This is where the distinction stops being theoretical — because when we misunderstand what these diseases are, we misunderstand what they are doing inside the body.

Nowhere is that disconnect more consequential for many, than in pregnancy, fertility, and early development.

Pregnancy, Fertility, and Fetal Development

One of the more grounding realities is how these diseases influence pregnancy, fertility, and early development.

Adenomyosis directly alters the uterine environment. It changes the structure of the muscle, the way the uterus contracts, and the vascular system that supports implantation. Chronic inflammation and immune changes can make implantation more difficult and influence pregnancy as it progresses.

This is reflected in increased risks of preterm birth, placental abnormalities, hypertensive disorders, and postpartum hemorrhage. Adenomyosis does not pause during pregnancy — it continues to shape the environment in which that pregnancy develops.

Endometriosis often impacts the process even earlier. It contributes to infertility through inflammation, anatomical distortion, and hormonal disruption. Even with assisted reproductive technologies, outcomes can be more complex.

When both conditions are present, those effects can compound. The focus cannot stop at whether pregnancy is possible. It has to include what happens after.

For years, these diseases were framed through reproduction alone. Pain was secondary. Immune dysfunction was barely studied. Pregnancy outcomes or complications never truly acknowledged. Research involving women was not consistently required until the 1990s — but things are slowly changing as move through the years.

Endometriosis and adenomyosis are now being recognized as complex, systemic, inflammatory diseases. We are not looking back at that shift. We are living in it daily. The last thirty years have brought more progress to women’s health than the centuries before them.

This does not end here — what we understand today is not final. It is a foundation. These outcomes are not separate from the disease itself. They are simply the disease being ignored and reduced. We have misunderstood these diseases because the system has insisted they were simple.

Where the Lines Begin to Blur

There is no cure for endometriosis. A hysterectomy, however, is a cure for adenomyosis since it is contained to the uterus. Treatments exist, but they are not perfect for either.

These diseases are complicated, and they are very real. I know this not just from research, but from my own life. As a teenager, I was told my pain was hysteria. Years later, after severe complications and multiple surgeries, I learned I had both endometriosis and adenomyosis — my uterus was removed.

The pain did not disappear all together. Some symptoms improved without the influence of what adenomyosis was doing alongside the endometriosis and other inflammatory triggers in my body.

When we finally separate normal tissue from disease, we begin to see it clearly. Endometriosis and adenomyosis are not weakness or basic women processes. They are chronic inflammatory diseases that deserve modern science, accurate definitions, and earlier recognition.

Pain that disables people is not normal, for anyone. The reality is finally being acknowledged and frameworks are shifting. The lining was never the same and neither was the disease.

The second annual American & Global College of Endometriosis Specialists (AGCES) took place in Las Vegas this year. It is a pioneering society dedicated to advancing care for endometriosis and adenomyosis, and one of the first to recognize the need for true subspecialty expertise in this space. The conference offers continuing medical education (CME) and Maintenance of Certification (MOC) credits for physicians and healthcare professionals, while also creating opportunities for students entering the field. Founded by Dr. Camran Nezhat, widely known as the father of modern video laparoscopy, alongside his brothers Dr. Farr Nezhat and Dr. Ceana Nezhat, the organization is rooted in decades of surgical advancement and evolving understanding of these conditions. They, with Barbara Page, also founded Worldwide EndoMarch; a global movement connecting patients and professionals through advocacy and public demonstration. The first march took place in Washington, D.C. in 2014, and over 2,000 people attended. There were 43 countries participating simultaneously, marking a shift toward visibility and collective demand for better care. AGCES continues in that same direction, working to expand education while pushing the field forward.

When I walked into AGCES 2026, I did not expect to see my own work reflected back at me.

I have spent years volunteering and collaborating within this space, and I was presenting two posters at this conference myself, so being part of the environment was not new. What caught me off guard was seeing my clinical puzzle — something I originally created as part of my article Endometriosis 101 for The Invisible Voice — appear within the opening presentation. It was not presented in my voice, and it was not directly credited to me beyond logos embedded within the images, but it was undeniably there.

What stayed with me was not simply seeing the slides themselves, but recognizing that the core argument behind them — the push to separate adenomyosis from endometriosis, to move beyond uterus-only imagery, and to frame endometriosis as a systemic disease — was being introduced without the full depth of the conversation that I actually created within. The visuals were there, but much of the harder nuance underneath them remained only partially explored or touched on.

Those slides were never meant to be simple awareness, visual graphics. They were built with intention beyond that article itself. They were designed to challenge the way we define and visualize endometriosis, while also introducing the complexity of adenomyosis. They were meant to push beyond simplified narratives and instead force people to sit in the discomfort of unanswered questions — particularly around biological differences, overlapping symptoms, historical assumptions, and the limitations of current representations.

At the center of that work I drew attention to a simple but often overlooked issue.

Uterus-only imagery does not represent everyone living with endometriosis, and continuing to rely on it reinforces a narrowed understanding of a condition that is far more complex. Many patients no longer have a uterus. Many never had uterine involvement at all. Many were told hysterectomy would cure them, only to continue living with disease on the bowel, bladder, diaphragm, nerves, abdominal wall, lungs, liver, and beyond.

At the same time, adenomyosis deserves its own language too. Adenomyosis is a uterine disease. Endometriosis is not. They are often grouped together, treated as interchangeable, and visually represented through the same symbol, but they are biologically different conditions that require different research priorities, different treatment pathways, and different conversations. Hysterectomy can be curative for adenomyosis and may bring profound relief. It does not cure endometriosis. That distinction is not semantics. It changes lives.

I know that personally.

In 2018, after more than fifteen years of dismissal, I finally received surgical confirmation of endometriosis and underwent excision surgery. I was still left navigating complications from disease damage and suspected adenomyosis. While recovering and trying to rebuild after surgery, I became pregnant. In 2021, after developing severe anemia during a high-risk pregnancy and nearly dying for the second time, I underwent a hysterectomy just four months after delivering my newborn to treat severe adenomyosis. It improved my quality of life and it treated adenomyosis — but it did not cure my endometriosis. Endometriosis was found for the second time in less than two years from the first and excised during that same surgery. Ongoing complications from disease and Ehlers-Danlos syndrome developed into prolapse concerns and into a surgery in 2023 for rectal prolapse repair and colo-resection. These complications and comorbidities eventually led to a yet another endometriosis specific surgery in 2025, where 17 adhesions, recurrent disease, and a new diagnosis of endosalpingiosis were discovered — another condition of cells similar to the fallopian tube are found outside of the tubes, considered to be within the same broader disease family of adenomyosis and endometriosis.

My disease has lived on my bowels, nerves, bladder, liver, and beyond. That is why seeing endometriosis constantly reduced to uterus-only imagery has been deeply difficult to navigate. Adenomyosis deserves the uterus symbol. I carry that loss proudly. But the rest of my body and the rest of my story — and so many others — is so often left out of the imagery, the conversation, and even the medical literature. I am not alone in that omission.

Representation matters because representation shapes science. If the disease is framed incorrectly, the biology gets studied incorrectly. If the biology gets studied incorrectly, treatment gets built incorrectly. If treatment gets built incorrectly, patients spend decades paying for the consequences. This is not a soft conversation about branding or awareness aesthetics. It is a clinical issue. It is a research issue. It is a policy issue. When research starts from the wrong framework, every patient downstream feels it.

That was the real purpose of the clinical puzzle. Not to make prettier education slides, but to challenge the foundation itself. To ask whether we are still teaching a disease through outdated symbols that no longer reflect what the evidence — and patients — have been saying for years. Seeing those slides used to open the conference, and then again to close it later on, created a complicated moment for me. A recognition that the conversation had moved forward, while also realizing how much of the deeper work was still unfinished.

Over the next few days, I sat in a room filled with surgeons, researchers, leaders in the field, and patients, listening as the nuance embedded within those ideas was only partially explored. At times it surfaced in presentations. At times it came through in Q&A discussions. At times it felt like it was still being worked through in real time right in front of me.

This is where I want to step in with my own perspective. Not to dismiss the progress that is happening, because there is meaningful advancement across many areas, but to sit honestly within that tension. To acknowledge what is working while also addressing what still feels misaligned. As these conversations move toward artificial intelligence, advanced diagnostics, and evolving surgical techniques, we also have to ask what information those systems are being built on — and whether we are truly moving forward, or simply carrying the same gaps with us into the next phase.

What Are We Actually Looking At?

There is a tension that runs through this field continuously — something that became impossible to ignore over the course of the conference.

What is endometriosis, and where does adenomyosis fit within that understanding? What is this biological language that still feels missing?

Both were discussed throughout AGCES, not as isolated topics, but as overlapping realities. There were conversations around imaging, surgical access, fertility outcomes, and disease progression. Yet even within all of that, the distinction between these conditions often felt blurred in ways that matter more than we tend to admit. While they are connected in some way, they are not identical. They are also not identical to what they have been affiliated with for over a century — the uterine lining itself. That difference is not minor. It shapes diagnosis. It shapes treatment. It shapes outcomes.

The clinical puzzle I created was built around that exact discomfort you see, the need to think beyond the uterus and question what we have long accepted as fact. The recognition that similarity does not equal sameness, and that shared pathways, hormonal responses, or visual markers do not erase biological nuance. If we are still asking whether these diseases are being defined correctly, then everything built on top of that definition matters too.

Sitting in that room, watching these ideas surface again in different forms, I couldn’t ignore the feeling that we are still circling something we have not fully named. At the same time, there is no denying that progress is happening. You can feel it in the room.

Artificial intelligence is no longer theoretical in these spaces. As of March 2026, the FDA has cleared or approved over 1,400 artificial intelligence and machine learning-enabled medical devices. What once felt distant is now being actively integrated into surgical environments — systems trained to recognize anatomy in real time, flag risk, preserve critical structures, and improve surgical precision where limited visibility or experience might otherwise create harm.

There were even discussions of tools that could pause or redirect surgical instruments when approaching high-risk anatomy, acting as built-in safeguards. Beyond the operating room, AI is also being explored through clustering models that combine patient-reported data and clinical findings to identify potential subtypes of disease and support more systemic evaluation. One early example discussed was the Nezhat Risk Advisor App, released in October 2019, designed as a screening tool to help patients identify elevated risk for endometriosis and potentially shorten the path to diagnosis and care before surgical confirmation ever occurs.

These developments are exciting. They hold real potential to reduce dismissal, reduce harm, and create more consistent pathways for patients who have long been left navigating uncertainty. The comparison that stayed with me was simple but effective — AI as an instrument panel for a pilot, not replacing the surgeon, but supporting a safer landing.

But even in that moment of advancement, there were questions brewing just beneath the surface. What are these systems being trained on, and by whom? How are procedures and risks being communicated to patients as these tools are introduced? Do these models account for the full variability of disease – differences in organ placement, anatomical variations, prior surgeries, hormonal complexity, and the wide range of symptoms that often fall outside traditional expectations?

Artificial intelligence does not create understanding. It reflects it. If we are still debating the biology of endometriosis itself – what is endometriosis, what is adenomyosis, where those boundaries begin and end – then we have to ask what it means to build intelligent systems on top of that uncertainty.

Those questions would return later in the conference, in a much different way.

Precision, Risk, and the Reality of Surgery

Surgery remains the center of everything. It is still considered the gold standard in this space, even as newer guidelines, such as those from ACOG, begin to emphasize clinical diagnosis. Excision surgery is where answers are confirmed, where disease is finally seen, and where action is physically taken at the root. But that outcome is never guaranteed — it depends entirely on the skill, knowledge, and experience of the person performing it.

Dr. Farr Nezhat spoke directly to this, acknowledging the limiting factors of surgery like anatomical knowledge, technical ability, access to proper instrumentation, and even familiarity with the devices and energy sources being used. There was an undeniable level of expertise in a room like that. It is something you feel as much as you observe — the refinement of technique, the confidence in movement, and the precision developed over years of practice.

Minimally invasive approaches, including laparoscopy and robotic-assisted surgery, were discussed in depth, particularly their ability to reduce hospital stays, minimize pain, and shorten recovery time. In some cases, robotic laparoscopy has even shown reduced operating times in patients with higher BMIs. And yet, as Dr. Camran Nezhat pointed out, two surgeons working in adjacent operating rooms can approach the same case with different techniques and still produce entirely different outcomes. That nuance matters. It reinforces that even within a “gold standard,” variability is built into the system.

To address that, many surgeons described reviewing their own procedures the same way athletes study game footage — replaying surgeries to identify patterns, refine technique, and reduce error. It is a practice rooted in accountability, but it also highlights something that cannot be ignored: complications are not rare, and they are not always minor.

Vascular injury was spoken about openly, not as an exception, but as one of the most common risks. Bleeding complications were highlighted in large-scale data involving more than 1.6 million surgeries, showing clear associations with longer hospital stays and increased recovery burden. But bleeding is only one part of a much broader picture. Incomplete resection remains a persistent concern, especially in complex cases where disease may be left behind or vital structures placed at risk during removal. In deep infiltrating endometriosis, the margin for error becomes even smaller. Precision becomes critical as the risks expand to include damage to surrounding organs, including the bowel, bladder, ureters, pelvic nerves, diaphragm, and major vascular structures.

More advanced procedures, such as colorectal resections involving the bowel, carry their own weight. Even when performed appropriately, they come with real and measurable risks, including serious complications like abnormal connections forming between organs—such as between the rectum and vagina — scar tissue that narrows normal function, and long-term changes that affect bowel, bladder, and sexual health.

Nerve injury adds another layer of complexity. Damage to major pelvic nerves— particularly the hypogastric nerves, which help regulate bladder, bowel, and pain pathways — can lead to persistent urinary dysfunction, difficulty emptying the bladder, and in some cases the need for long-term catheterization.

Diaphragmatic endometriosis introduces an entirely different level of risk. When disease involves the diaphragm or areas near the lungs, surgical intervention can affect respiratory function, sometimes resulting in complications like collapsed lung (pneumothorax) or long-term breathing difficulties if the phrenic nerve — the nerve that helps control breathing — is impacted.

Even when surgery is considered “successful,” the story does not always end there. Chronic pain can persist or return, driven not only by residual disease, but by immune dysregulation and long-term sensitization of nerve pathways. These are the outcomes patients are often left navigating long after the operating room is cleared. Many surgeons are still not trained to fully recognize the whole-body impact this disease can carry.

This is not meant to diminish the importance of excision surgery — it remains one of the most effective tools we have. It is a reminder that surgery is not a cure-all, and it is not without risk.

The outcomes are shaped by the person performing it including their training, their experience, and their interpretation of what they are seeing in real time. It also depends on an individualized approach to each patient. That means outcomes are not just medical. They are variable, and patients live within that variability every day.

When Access Determines Outcome

That variability becomes even more significant when placed in a global context. Out of a population of more than eight billion people, an estimated five billion lack access to safe or adequate surgical care. Nearly 65% of the global population lives within a balance of risk and potential harm created by gaps in training, education, surgical precision, and access to updated medical practice. It is estimated that 143 million additional surgeries are needed each year worldwide, and that approximately 19 million deaths could be prevented with proper surgical intervention.

In endometriosis, those numbers stop being abstract very quickly.

This disease is not confined to a single organ. It can involve the bowel, bladder, ureters, diaphragm, lungs, nerves, pelvic sidewall, vascular structures, and multiple overlapping systems throughout the body. Surgical treatment is often not simply gynecology—it becomes colorectal surgery, thoracic surgery, urology, neuropelveology, and complex multidisciplinary care happening at once.

The difference between a provider who recognizes that complexity and one who does not can mean the difference between preservation and permanent damage.

Lower surgical skill does not just increase recurrence risk. It increases the risk of incomplete excision, preventable organ injury, repeated operations, unnecessary hysterectomies, fistulas, nerve damage, urinary dysfunction, respiratory complications, and lifelong disability. Precision becomes smaller as disease complexity expands.

This is part of why classification matters. The recent AGE Classification System emphasizes that surgical staging must reflect real disease burden, anatomical involvement, and operative complexity rather than relying on oversimplified frameworks that fail to capture patient reality. When classification is inaccurate, treatment planning becomes inaccurate too.

When placed alongside everything else discussed at the conference —innovation, artificial intelligence, earlier detection, and precision-based surgery — this reality becomes harder to ignore. Surgery may be advancing, but access, consistency, and training remain just as critical to outcomes as the techniques themselves.

Until those gaps are addressed, the gold standard will continue to mean very different things depending on who is on the other side of the instrument.

A Disease That Refuses to Stay in One Place

One of the most consistent undercurrents throughout the conference was just how extensively endometriosis can involve the full body system. For decades, it has been framed as a condition confined to the uterus or, at most, the pelvic cavity. That framing alone has set the field back, limiting both how the disease is recognized and how it is treated. The discussions at AGCES made it clear, this understanding is no longer sufficient, yet the broader narrative has not fully caught up.

Adenomyosis, by definition, is uterine-based, existing within the myometrium. But even here, the conversation does not remain simple. There is significant overlap between adenomyosis and endometriosis, not just in symptoms, but in inflammatory response and disease behavior. This overlap is not rare or incidental — it is frequent enough to challenge the idea that these conditions can be cleanly separated in practice. It challenges any similar straight-angle of the endometrium for either condition. Yet, while they intersect, they are not the same, which makes the need for biological clarity even more important.

Then there is the question of location, which continues to expand what we thought we understood. The urinary system was repeatedly referenced as one of the more common sites of endometriosis involvement beyond traditional expectations, with symptoms that can mimic entirely different conditions and delay recognition even further. Deep infiltrating endometriosis brings the disease into spaces where anatomy becomes distorted, where fibrosis and adhesions reshape structures, and where surgical intervention carries significantly higher risk. These are not isolated or rare presentations. They are part of the disease’s behavior.

Beyond that, the reach becomes even harder to ignore. Endometriosis has been documented in the bowel, affecting areas like the sigmoid colon, rectum, and small intestine, often leading to impaired function, chronic pain, and a significant decline in quality of life. It has been identified within the rectovaginal septum and along pelvic sidewalls, creating layers of complexity in both symptom presentation and surgical management. In some cases, it extends even further. Into the diaphragm, where involvement can affect breathing and present as fatigue, shortness of breath, or recurring respiratory complications. These are not symptoms patients, or even many providers, are initially taught to associate with endometriosis.

Many patients and advocacy spaces use the term extra-pelvic endometriosis to describe disease beyond the uterus, but anatomically, extra-genital may often be the more accurate term. Bowel, bladder, ureter, and rectovaginal disease can remain within the pelvic cavity while still existing far outside reproductive structures. Truly extra-pelvic disease — such as diaphragmatic, thoracic, pulmonary, or abdominal wall involvement — extends even further. What becomes even more difficult to reconcile is that in certain rare cases, these manifestations carry risks beyond dysfunction. These cases have been shown to become aggressive, involving cancer changes in endometriosis, challenging the long-standing tendency to frame endometriosis as entirely benign without acknowledging the full clinical reality.

What stood out was not just the presence of this data, but the disconnect surrounding it. In specialized rooms like AGCES, there is growing acknowledgment that endometriosis extends beyond the pelvis, that it can involve multiple organ systems, and that its presentation is far more complex than historically defined. Yet, for many patients, the first explanation they receive still does not reflect that reality. Surgeons note that they are taught to look in one place, for one type of symptom, within one limited framework.

The body does not compartmentalize this disease. We do. That gap continues to cost people time, appropriate care, and clarity in understanding what is happening within their own bodies.

This Is Not Benign

There were moments throughout the conference where the language we use to describe endometriosis specifically began to feel increasingly limited. It is often referred to as a “benign” condition, but after sitting through multiple discussions and data points, that word does not always seem to capture the full scope of what is being observed.

Conversations around malignant transformation were not always the main focus of a presentation, but they were present enough, and consistent enough, to stand out. Endometriosis has been shown to undergo malignant transformation in a small percentage of cases, estimated to occur in roughly 1% to 2% of those affected. While that number may appear low at first glance, it becomes more complex when placed within the broader biological context of the disease.

The majority of these transformations are associated with ovarian cancers, particularly endometrioid and clear cell subtypes, both of which have been repeatedly linked to endometriosis. These are not incidental findings. They are supported by biological evidence showing that chronic inflammation, repeated tissue injury, oxidative stress, and long-term cellular damage can create an environment where abnormal cells are more likely to grow and survive.

Researchers have identified shared molecular changes in some of these cases, including mutations in genes such as ARID1A, PTEN, and KRAS — genes involved in how cells repair damage, regulate growth, and prevent abnormal development. In simple terms, this means the relationship is not just observational. There are biological pathways helping explain why this connection exists.

What expands the conversation even further is the presence of extraovarian malignancies. Endometriosis-associated cancers have been documented in locations beyond the ovary, including the bowel, bladder, ureters, and even within surgical scars. These cases are rare, but often aggressive, and they challenge the long-standing assumption that endometriosis exists only within a contained, predictable space. In some instances, these malignancies develop in areas where endometriotic lesions have already been identified, reinforcing the idea that location does not limit potential impact.

When viewed alongside earlier discussions at the conference — systemic spread, chronic inflammation, immune dysregulation, and the ability of endometriosis to exist in multiple organ systems — these findings begin to feel less like isolated exceptions and more like part of the same biological continuum. The same environment that contributes to pain, infertility, and disease progression may also, under certain conditions, contribute to cellular changes over time.

Hearing these connections presented in a clinical setting carries a different weight. It shifts the understanding of endometriosis beyond something that simply causes symptoms, and to something that exists within a broader and more complex biological framework. One that includes not only where the disease is found, but how it behaves over time.

It also raises important questions about how often endometriosis is still minimized in both public and clinical conversations. When the focus remains limited to pain or fertility alone, it overlooks the deeper mechanisms that are actively being studied and discussed within specialized spaces. It creates a gap between what is being learned and what is being communicated.

This is not about creating fear, it is about creating accuracy. Understanding the full scope of a disease — especially one that has historically been misunderstood — requires acknowledging both its common presentations and its more serious, less discussed possibilities. It requires recognizing that while malignant transformation is not the typical course, it is still a documented one, and one that deserves appropriate awareness, surveillance, and continued research.

If the goal is earlier detection, better outcomes, and more informed care, then these conversations cannot remain at the edges. They have to be part of how we define and approach the entirety of this disease moving forward.

Pregnancy, Fertility, and Fetal Development Impact

One of the more grounding moments throughout the conference came through repeated discussions on pregnancy and fetal development, particularly in relation to both endometriosis and adenomyosis. This was not always presented as a standalone topic, but it surfaced consistently — woven into presentations, reinforced through questions, and revisited in ways that made it difficult to overlook.

Adenomyosis, in particular, was brought forward in a way that deserves far more attention than it typically receives. Traditionally, it has been described as endometrial-like tissue growing into the muscular wall of the uterus. But even that definition is beginning to feel less settled. Some continue to describe it as the uterine lining itself extending inward, while others, including perspectives emphasized by the Nezhat approach, urge that it is more accurate to consider it as similar to endometrial tissue rather than identical. That distinction may seem subtle, but it carries weight. It reflects a broader shift happening across this field, moving away from assumptions that have been held for decades and toward a more biologically precise understanding of what these tissues actually are.

What is not debated is the environment adenomyosis creates. Because it exists within the myometrium, its influence on pregnancy is direct. It alters the structure of the uterus, the way it contracts, and the vascular environment that supports implantation and early development. Chronic inflammation and immune dysregulation create conditions that can make successful implantation more difficult and may continue to influence the pregnancy long after it begins. These are not abstract concerns. They are reflected in increased risks of complications such as preterm birth, placental abnormalities, hypertensive disorders in pregnancy, and postpartum hemorrhage. In this context, adenomyosis does not pause during pregnancy. It remains present, actively shaping the conditions in which that pregnancy develops.

Endometriosis carries its own set of challenges, often beginning earlier in the process. It is one of the leading contributors to infertility and data shows factors in unexplained infertility affecting a significant portion in individuals. The mechanisms are layered — chronic inflammation disrupting fertilization, anatomical distortion from adhesions affecting the fallopian tubes and ovaries, and hormonal signaling that can interfere with ovulation and endometrial receptivity. Even with assisted reproductive technologies, outcomes can be more complicated, with lower success rates and higher risks of miscarriage reported in comparison to those without the disease.

When these two conditions coexist, as they often do, the impact can compound. The inflammatory environment, structural changes, and hormonal disruptions do not exist in isolation. They build on one another, influencing not only the likelihood of conception but the stability of pregnancy itself. There were discussions that pointed toward increased risks of very preterm birth in these combined cases, reinforcing that the overlap between endometriosis and adenomyosis is not just a diagnostic challenge, but a clinical one with real consequences.

What stood out was not just the data, but how often these realities had to be pulled into the conversation rather than centered within it. Questions brought the focus back to fetal development, to pregnancy outcomes, to what happens after conception — not just whether conception is possible. That distinction matters. Because too often, the conversation around endometriosis stops at fertility, without fully acknowledging what patients may face beyond that point.

There was also a clear recognition that adenomyosis remains underdiagnosed, particularly within obstetrical care. Recommendations were made for earlier documentation, improved imaging during initial prenatal visits, and stronger communication between specialists. These are practical steps, but they also highlight how much of this understanding is still being integrated into standard care.

When we describe these conditions as chronic, systemic, and inflammatory, that definition cannot stop at pain or infertility. It has to include the uterine environment, the immune response, and the developmental conditions that exist before a child is even born. In some discussions, adenomyosis was even referred to as a form of fetal environmental influence, a framing that underscores just how early these effects may begin.

These are not secondary considerations, they are part of the full picture. If we are continuing to fine-tune how we define these diseases at a biological level, then we also have to be willing to follow that definition all the way through its impact — into the earliest stages of life and across the lifespan.

A Broader Pattern: Fibroids and PCOS

While much of the conference centered around endometriosis and adenomyosis, fibroids were also a consistent point of focus — quietly reinforcing just how interconnected these conditions truly are. Fibroids remain one of the most common gynecological conditions, affecting an estimated 70% to 80% of women by the age of 50. Their impact is not minor. Heavy menstrual bleeding, anemia, chronic pain, pressure symptoms, and reduced fertility all shape patient outcomes in ways that extend far beyond the uterus itself. The economic burden alone reflects how widespread and disruptive this condition has become.

Yet, despite that prevalence, the patterns surrounding fibroids felt familiar with delayed diagnosis, multiple providers before answers are found, and the limited discussions around full treatment options or long-term management. These are clearly not isolated to one condition. They are systemic.

There were meaningful conversations around how fibroids are managed, including minimally invasive procedures like uterine artery embolization, surgical options such as myomectomy, and stronger emphasis on multidisciplinary care models. The concept of coordinated fibroid care — bringing together surgical specialists, interventional radiology, reproductive medicine, pain management, and medical management — offered a glimpse into what more integrated care could look like.

For the patient, that kind of model changes everything. Instead of moving between disconnected appointments, repeating the same history to multiple providers, and being forced to piece together treatment plans alone, care becomes collaborative. Decisions are made with a fuller understanding of fertility goals, symptom burden, surgical risk, long-term quality of life, and the reality that these conditions rarely exist in isolation.

In many ways, that is the same gap endometriosis patients continue to navigate. Too often, treatment remains fragmented — gynecology separated from colorectal care, pelvic pain separated from urology, fertility separated from systemic disease. The burden of coordination falls back onto the patient. Seeing fibroid care discussed through a more multidisciplinary lens offered a practical example of what should not be exceptional, but standard.

There was also attention given to lifestyle and metabolic factors. Nutrition, inflammation, and broader health patterns were discussed as contributing elements in fibroid development and progression. These conversations mirror many of the same pathways being explored in endometriosis and adenomyosis, reinforcing the idea that these conditions do not exist in isolation. They exist within a shared biological and systemic environment.

At the same time, the lived experience data told a similar story. Patients often delay seeking care for years. Many see multiple clinicians before receiving a diagnosis. Stress, uncertainty, and lack of clear guidance remain common threads. And perhaps most telling, a significant number of patients report never having meaningful conversations about their reproductive goals as part of their treatment planning.

When conditions like fibroids, endometriosis, and adenomyosis intersect as they often do — the need for comprehensive, individualized care becomes even more critical. Not just treating one diagnosis at a time, but understanding how these conditions overlap, influence one another, and shape outcomes across a patient’s lifetime.

This pattern does not stop with fibroids. Conditions like Polycystic Ovary Syndrome were not a central focus of the conference, but their presence is impossible to ignore within the broader landscape of gynecologic health. PCOS remains one of the most common endocrine disorders affecting reproductive-age women and is increasingly understood not as an isolated ovarian condition, but as a lifelong metabolic and hormonal disease.

Like endometriosis and adenomyosis, PCOS exists at the intersection of inflammation, hormonal dysregulation, and even metabolic dysfunction. It carries its own patterns of delayed diagnosis, inconsistent screening and long-term health risks. This may include diabetes, cardiovascular complications, and adverse pregnancy outcomes. Even patients without obvious external markers who are often referred to as “lean PCOS”, can experience the same underlying disruptions, further complicating recognition and care.

While these conditions are often approached as separate diagnoses, they are frequently shaped by the same underlying pathways and managed within the same fragmented systems of care — further blurring the lines between what has traditionally been treated as distinct.

The Quiet Push Toward Earlier Detection

There were moments during the conference that felt like a glimpse into what could come next. They weren’t always the loudest discussions, but they carried a different kind of weight. Conversations around the microbiome, inflammatory markers, and molecular signatures continued to surface, pointing toward the possibility of identifying endometriosis without relying solely on surgery — or at least before the disease progresses to the point where surgical intervention becomes unavoidable.

That shift feels long overdue. Endometriosis continues to carry an average diagnostic delay is at an estimated 6-12 years in the United States. With many patients seeing multiple providers before receiving an answer. In some cases, particularly among adolescents, that delay begins early and stretches across critical developmental years. These gaps are not just inconvenient — they shape disease progression, influence fertility outcomes, and contribute to the chronic nature of pain that so many patients experience.

There was a clear emphasis throughout the conference on why earlier detection matters. Identifying the disease sooner has the potential to reduce long-term morbidity, limit progression, and improve overall quality of life. It also begins to shift the conversation away from reactive care and toward something more proactive — something that acknowledges the disease before it has had years to evolve unchecked.

At the same time, there is a growing wave of innovation attempting to meet that need. One of the most notable developments, discussed by Dr. Gaby Moawad, was the use of saliva-based microRNA signatures, analyzed through artificial intelligence, as a non-invasive diagnostic approach for endometriosis. Unlike traditional pathways that often rely on surgical confirmation, this model is built on identifying molecular patterns — 109 specific microRNA markers derived from patient saliva samples — designed to distinguish between those with and without disease.

Early validation data shows strong diagnostic performance, with sensitivity and specificity expected to reach or exceed 90%, and the ability to detect disease even in patients with suspected but not yet surgically confirmed endometriosis. What makes this particularly significant is not just the accuracy, but the structure of the study itself. Patients included were already navigating real clinical pathways — undergoing imaging, multidisciplinary evaluation, and in many cases preparing for surgery — meaning the model is being tested within the same environments where diagnostic uncertainty already exists.

Importantly, the model does not rely solely on symptom-based reporting. It is anchored, in part, to surgically confirmed disease through expert biopsy validation, strengthening its clinical relevance and addressing a long-standing limitation in endometriosis research, where suspected diagnosis and confirmed pathology have not always been clearly separated. That distinction matters — especially in a field where diagnostic ambiguity has historically shaped both research outcomes and patient care.

A tool like this has the potential to shift endometriosis from something that is confirmed late — often after years of progression — to something that can be identified earlier, more accessibly, and without immediate reliance on invasive procedures. It opens the possibility of triaging patients within primary care settings, reducing the diagnostic gap that has defined this condition for decades, and potentially altering the trajectory of disease progression before it reaches surgical complexity.

But even within that promise, there are limitations that cannot be overlooked. The study population is specific — patients already within specialized care pathways, aged within a defined range, and often presenting with moderate to high suspicion of disease. While the accuracy remains strong across both early-stage and more complex disease presentations, questions of generalizability remain, particularly in adolescents and more diverse patient populations. There is also the reality of false negatives — patients with negative biopsies who may still have disease that was not captured — as well as overlapping histological findings, such as fibrosis, that can complicate interpretation.

Even among those closely following this work, the response reflects that same balance. There is real recognition of how far this has come, especially in achieving strong diagnostic performance across disease stages and grounding the model in surgically validated cases.

After the presentation, I asked directly about the model itself and how these markers were being identified and validated in relation to actual biological endometriotic tissue — whether the signatures were being anchored back to confirmed disease at a tissue level, or built primarily through pattern recognition across symptomatic populations.

The answer was brief. I was told to reference the full study, and that it was behind a paywall. It wasn’t a dismissal so to speak, but it was a reminder. Access to information matters just as much as the innovation itself. Especially in a field where patients, advocates, and interdisciplinary researchers are actively trying to bridge gaps that have existed for decades. The ability to question, review, and understand how these models are built is not separate from progress — it is part of it.

Looking deeper into the protocol, the complexity becomes clearer. This is not a simple screening tool. It is a multicenter, longitudinal study built on patients already within clinical care pathways, combining molecular data with imaging, surgical outcomes, and quality-of-life reporting. It is structured, layered, and still evolving.

What began as a conceptual shift quickly moved to something more tangible. Not just why earlier detection matters — but how it might actually be achieved.

What We See, What We Miss

Imaging held its own weight in these conversations as well, particularly in the ongoing tension between ultrasound and MRI as primary tools for detection. Both were presented as valuable, but in very different ways.

Ultrasound especially when performed by experienced specialists, was emphasized as a dynamic, accessible tool. Techniques like the “sliding sign” and tenderness-guided transvaginal ultrasound allow clinicians to assess organ mobility, adhesions, and deep infiltrating disease in real time. It is cost-effective, widely available, and capable of being integrated earlier into patient care pathways.

MRI, on the other hand, was positioned as a more comprehensive mapping tool. Its ability to visualize deeper disease, particularly in areas like the bowel, bladder, and upper abdomen, makes it valuable for pre-surgical planning and for identifying involvement beyond the pelvis. It provides a level of anatomical detail that ultrasound may not always capture, especially in more complex cases.

What stood out most wasn’t which tool was better. It was the variability between them.

Ultrasound is highly operator-dependent. Its accuracy relies heavily on the skill, training, and experience of the person performing it. In the right hands, it can rival more advanced imaging. In the wrong setting, disease can still be missed entirely. MRI offers more consistency in interpretation, but comes with higher cost and reduced accessibility, limiting its role in early, widespread detection.

The debate itself reflected something larger. We are not just choosing between technologies — we are navigating the gap between what is possible and what is accessible. Even with advanced imaging, significant disease can still go undetected, particularly outside of specialized centers.

While artificial intelligence is beginning to integrate into imaging assisting with lesion identification, segmentation, and predictive modeling — it is still being layered into systems that depend on both human interpretation and structural access.

Which brings imaging back into the same conversation as everything else. Earlier detection is not just about having better tools. It is about where those tools exist, who is trained to use them, and whether patients can realistically access them before the disease progresses.

Beyond imaging, digital tools are beginning to shape how patients interact with their own data. Mobile applications designed to assess risk, track symptoms, and map pain patterns over time are being introduced as a way to bridge the gap between patient experience and clinical evaluation. Some aim to simulate risk profiles or cluster symptoms in ways that may help predict disease involvement before surgery is ever considered.

At the research level, even more advanced models are being developed, including “organ-on-chip” technology mentioned by the NIH and biomarker-driven systems intended to better replicate human biology in ways traditional models have struggled to achieve. Organ-on-chip are small laboratory devices designed to mimic how human tissues and organs actually function. Instead of relying on only animal models or simplified cell cultures, researchers can use living human cells arranged in microfluidic chips that stimulate blood flow, hormone signaling, inflammation and tissue interaction in real time. In endometriosis research, this creates the possibility of studying how lesions behave, how inflammation spreads, how immune responses shift, and how treatments respond in a system that more closely reflects the human body.

This matters because one of the longest standing problems endometriosis research has been the gap between what we observe clinically and what traditional laboratory models can accurately reproduce. If the model itself is incomplete the conclusions often are too. Technologies like organ-on-chip systems offer a chance to study disease progression earlier, test therapies more precisely and potentially identify biomarkers before surgical intervention becomes necessary.

On the surface, these developments feel like progress — and in many ways, they are. But they also bring us back to familiar questions. If we are building new diagnostic pathways, what are they being built on? How are different presentations of disease being represented in the data? Are we capturing the full spectrum of what endometriosis and adenomyosis actually look like — or refining systems around an already limited framework?

Earlier detection is not just about finding the disease sooner. It is about finding it accurately. Without that level of precision, earlier detection risks becoming another layer built on incomplete understanding. Even then, accuracy alone does not determine impact. Questions of accessibility, cost, and clinical integration remain just as important. If access is limited — or if surgical intervention is still required for treatment regardless of detection — then these tools become part of a larger diagnostic ecosystem rather than a complete solution on their own.

That space matters here too. There were important acknowledgments around disparities in diagnosis — particularly for adolescents and non-white patients — who continue to face longer delays and reduced access to minimally invasive diagnostic pathways. These are not separate issues. They are part of the same system that has historically struggled to recognize and respond to this disease in a timely and equitable way.

The current model where patients wait years for confirmation, rely on progression, and often dismiss symptoms until they become severe is not, nor has ever been sustainable. It never was to begin with really. If the field is moving toward earlier, less invasive ways of identifying endometriosis, then the opportunity is not just to improve timing. It is to reshape how the disease is understood from the very beginning.

Progress, With Friction

There was no question that progress was happening throughout the conference. You could feel it in the advancements being presented, in the conversations around technology, and in the shared goal of improving outcomes. But alongside that progress, there were moments where something didn’t fully align. Not enough to stop the conversation, but enough to create a kind of friction that was hard to ignore.

One of those moments came through the continued reliance on long-standing theories that, while historically foundational, may no longer fully explain what we are seeing. Retrograde menstruation was still referenced as a primary mechanism in the development of endometriosis. Originally proposed by Sampson nearly a century ago, the theory suggests that endometrial cells travel backward through the fallopian tubes during menstruation and implant throughout the pelvic cavity.

The problem is that retrograde menstruation occurs in the majority of menstruating individuals, while only a fraction develop endometriosis. It also fails to explain documented cases in fetuses, premenarchal children, postmenopausal patients, individuals without a uterus, cis men, and extra-pelvic disease involving distant organs such as the lungs or diaphragm. For decades, these contradictions have challenged the idea that retrograde menstruation can serve as a complete origin theory rather than one possible contributing mechanism.

Even within the same space, there were discussions that pushed beyond that explanation. Conversations around cellular behavior, molecular differences, immune dysfunction, stem-cell theories, Müllerian remnants, coelomic metaplasia, and systemic inflammatory involvement point toward something far more complex than simple displacement of uterine lining. When we begin to recognize differences in tissue behavior, inflammatory response, and disease presentation across multiple organ systems, it becomes harder to rely on a single origin theory without questioning its limitations.

That tension is not just theoretical. It extends into the language we use. Terms like “endometrial” and “endometriotic” are often used interchangeably, but they are not describing the same thing. Endometrial tissue refers to the normal lining of the uterus. Endometriotic lesions behave differently — molecularly, immunologically, and clinically. That distinction matters more than it may seem on the surface.

Language shapes research. It shapes diagnostics. It shapes how data is categorized, interpreted, and now, increasingly, how artificial intelligence systems are trained to recognize patterns and disease. If we are still using terminology that assumes sameness where there may be biological difference, then we risk reinforcing those assumptions at scale — not just in conversation, but in the datasets and models being built to define the future of diagnosis and care.

Asking the Question Out Loud

Toward the end of the conference, during a discussion centered on research models, I asked a question that had been building all weekend. Much of the presentation by Dr. Stacy McAllister leading up to that moment focused on animal models, particularly mouse and rat models, where endometriosis is surgically induced and then studied in controlled environments. These models are widely used to explore disease mechanisms, from inflammation and immune response to hormonal signaling and pain pathways. They allow researchers to isolate variables, test interventions, and begin to understand processes that are difficult to observe directly in human populations. In many ways, they are foundational to how current therapies are developed and evaluated. There is value in that work.

Rodent models have contributed to important insights, including the role of oxidative stress, immune dysregulation, and molecular pathways involved in pain and lesion development. They have helped identify potential therapeutic targets and supported the development of both hormonal and non-hormonal treatment approaches. In some cases, findings across species have shown overlap, reinforcing certain biological patterns that appear consistent. But as the discussion unfolded, it became harder to ignore the gap between what is being created in a controlled setting and what occurs naturally in the human body.

These models are built through surgical implantation or genetic modification. They rely on controlled conditions, altered immune environments, and simplified systems that do not fully reflect the variability, complexity, or origin of endometriosis as it develops in humans. Even the most advanced models — those using human tissue — often lack the full immune interaction that is central to how this disease behaves over time.

I was waiting to be called, and then the question was asked about using animals where naturally developing tissue occurs, such as macaques (monkeys) and if they had looked into this route of testing. There were discussions of ethical limitations — what can be studied, what cannot, the price and how those boundaries shape the direction of research itself.

I was eager to ask my question especially after this discussion, and finally I was called on and I asked:

“I know the biological differences between the native and actual endometriosis tissue – being very distinct and different – so how is that going to be representative across future studies and research using these kind of models and how could have an impact on what we are shifting towards in patient or human representation?”

It wasn’t asked to challenge per se, it was asked because the answer matters.

Dr. Stacy McAllister began to state that the difference in ALDH2 reduction or whatever was acting before in the eutopic and ectopic samples, is not going to be found in the rat models. We are dependent on that model of injected human tissue in a different environment where it is not occurring like it naturally is in women…..

Her answer was veering from what I was seeking, and I admittedly interrupted her there.

“So how can we say that the naturally occurring disease and the surgically stimulated disease is going to produce the same outcome?”

She shocked me with her response.

There were acknowledgements. Considerations of alternative models. Mentions of naturally occurring disease in other species, including those that develop endometriosis without intervention. It became clear that while these models offer insight, they may not fully capture the complexity, variability, and origin of the disease as it exists in real life. I was thrilled to be a part of that conversation of nuance backing up my clinical puzzle further.

What stood out most was not the answers, but the willingness to sit in that uncertainty and chat amongst a group of very skilled and impactful individuals. It wasn’t a closed answer or redirect to change the subject. This is how we move forward.

Building Intelligence on an Unfinished Foundation

As those earlier questions around artificial intelligence began to resurface, the conversation shifted. What initially felt like excitement around capability started to move into something more complex — something less about what these systems can do, and more about what they are built on.

Artificial Intelligence (AI) and Machine Learning (ML) is already showing up and being integrated into diagnostics, surgical planning, imaging, and even early screening tools. Systems designed to identify patterns faster than the human eye, to map disease progression, to assist in surgical precision, and to reduce the very delays that have defined this condition for decades.

There was a sense of momentum in those discussions. AI models analyzing imaging to detect lesions before surgery. Predictive tools mapping potential disease spread and surgical risk. Augmented systems guiding surgeons in real time, highlighting structures and improving precision in complex cases. Even non-invasive approaches, like saliva-based micro-RNA testing, showing accuracy levels that could fundamentally shift how early this disease is recognized.

It was impressive, it should be. The potential here is real. The ability to reduce diagnostic delay. To improve surgical outcomes. To move toward more personalized, data-driven care. To give patients answers sooner, and with less harm. But beneath that momentum, there was something else. A quieter question I kept coming back to.

“What are these systems being trained on?”

Because artificial intelligence does not create understanding. It reflects it. It learns from the data it is given — the definitions we use, the models we build, the assumptions we repeat. If those foundations are incomplete, inconsistent, or still evolving, then those same gaps risk being carried forward into the systems we are now beginning to rely on.

This is where the earlier conversations return.

If we are still debating the biological nature of endometriosis and adenomyosis…
If we are still navigating differences between endometrial and endometriotic tissue…
If we are still working to fully recognize the systemic and extra-pelvic nature of the disease…

Then we have to ask what it means to train these intelligent systems within that uncertainty. Precision depends on clarity. Yet that clarity is still being built. At the same time, there is opportunity here that cannot be ignored. Not all data lives in imaging or surgical reports.

Some of it lives in language. In patterns of symptom description or in the way patients communicate distress long before a diagnosis is ever made. That is where another layer of this conversation begins to emerge.

If artificial intelligence is going to help us detect this disease earlier, then it has to learn from more than just clinical confirmation. It has to include lived experience. It has to recognize patterns of delay, dismissal, and progression that exist outside of traditional datasets. Not just what the disease looks like once it is found, but how it presents before it is ever named.

There were early signs of that integration. With older and newer mobile applications, risk assessment tools, structured tracking systems attempting to capture patient-reported data and translate it into something actionable. Communication strategies and tracking systems that report immediately to your surgeon. Systems that aim to bridge the gap between symptom experience and clinical recognition. The programs discussed were jaw dropping, many focusing on integrating the Nezhat’s full data and resource library as well as their patient collections. But even that comes with responsibility. How we define symptoms, how we label conditions, and how we structure those inputs will directly shape what these systems learn to recognize.

Language matters. Definitions matter. The difference between something being similar and something being the same matters more than it may seem — especially when those distinctions are used to train models that will influence future diagnosis and care.

So while the advancement of AI and ML represents one of the most promising shifts in this field, it also reinforces something we cannot afford to overlook. Progress is not just about building better tools, it’s about making sure those tools are built on foundations strong enough to carry them forward.

Innovation Without Oversight

Alongside discussions of artificial intelligence, early detection, and emerging diagnostic tools, there was another layer of innovation that’s been gaining traction. One that felt less defined, but equally impactful. The growing conversation around GLP-1 receptor agonists and peptide-based therapies in endometriosis management.

These treatments are not being positioned as primary standards of care, but they are increasingly entering the discussion. GLP-1 medications, originally developed for metabolic conditions, are now being explored for their potential role in regulating inflammation and metabolic dysfunction — both of which are implicated in endometriosis. Some patients report improvements in symptoms. Others are still navigating what these effects mean long-term.

Peptide therapies are being discussed in a similar space. Compounds targeting inflammation, oxidative stress, mitochondrial function, and tissue repair are being explored as potential adjuncts to treatment. On a biological level, many of these mechanisms make sense. They align with pathways already recognized within the disease.

But that is where the clarity begins to shift. Unlike the structured clinical trials and validation pathways discussed in other parts of the conference, access to many of these therapies is not always occurring within the same level of oversight.

Patients are increasingly obtaining GLP-1 medications and peptide-based treatments through telehealth platforms, online vendors, and compounded sources that may not carry the same level of regulation, consistency, or verification. Documentation of compounding practices, dosing accuracy, and quality control is not always transparent. When that happens, the risk shifts. Not to the system, to the patient.

This is something I have raised beyond this conference as well, including in policy discussions around the regulation of compounded medications. While innovation can move quickly, oversight does not always move at the same pace. When emerging treatments begin to intersect with widespread access before sufficient evidence, regulation, or safety monitoring is in place, the burden of uncertainty is no longer theoretical. It becomes lived.

That does not mean these therapies should be dismissed. There is potential here. The mechanisms being explored are not without merit, and the interest in non-hormonal or adjunctive treatment pathways reflects a real need within the community. At the same time, that interest in non-hormonal approaches exists alongside a continued reliance on hormonal suppression strategies that remain central to post-surgical management.

One moment during a live-streamed surgical case brought that tension into focus. Toward the end of the procedure, during panel discussion, a question was raised from an international colleague about next steps in prevention — whether the patient would be placed on agonists or hormonal therapy in the months following surgery. The response reflected a familiar reality within U.S.-based care and beyond.

There was acknowledgment that many patients do not want to be on hormone modulators, and that recommending them can feel like a difficult conversation — one that some clinicians often feel they have to navigate carefully. Medications such as GnRH agonists and antagonists, along with other hormonal options, are described as tools to help reduce recurrence, but they fail to draw the context that the recurrence is not that of the disease, but of symptom recurrence and disease-related pain.

Another panelist added nuance, noting that age and reproductive goals matter. For patients actively trying to conceive, these treatments may not be recommended. For others delaying pregnancy, options like norethindrone or intrauterine devices are often suggested as part of a management plan. It was a thoughtful exchange. But it also highlighted something deeper to me.

While these medications are frequently positioned as a way to reduce recurrence, with no further context, the evidence behind that claim is not always as clear as it is presented. Much of the data focuses on symptom suppression or recurrence of cystic structures that are not consistently biopsied or confirmed as endometriosis at a tissue level. Broader disease progression — particularly in extra-pelvic or less visible locations — is not as well tracked within these frameworks. In a field where the biology of the disease is still being actively defined, that’s important.

At the same time, there is a growing body of concern around how some of this data has been interpreted and applied over time, including instances where foundational claims have been challenged or re-evaluated, yet continue to influence current clinical recommendations. These medications remain embedded within treatment pathways, including recent guideline updates, even as patient experiences and emerging data continue to raise questions about long-term outcomes, side effects, and overall effectiveness beyond symptom management.

Which brings the conversation back to the patient. The hesitation being described in that room — the reluctance to start hormonal therapy — is not occurring in a vacuum and not just limited to the United States. It reflects lived experiences, side effects, quality-of-life tradeoffs, and a broader awareness among patients who are increasingly becoming informed about their options and their risks. This is not simply resistance. It is decision-making. When that decision-making intersects with emerging therapies whether hormonal, metabolic, or peptide-based — the need for clear evidence, transparency, and individualized care becomes even more critical.

In the absence of that clarity, the burden of navigating these choices does not sit with the system. It sits with the patient. However potential does not replace evidence, and access without oversight is not the same as access to care. When treatments are introduced into patient populations without consistent regulation, validated dosing, or long-term safety data, outcomes become unpredictable. Some patients may experience relief. Others may experience harm. Without structured systems in place, both outcomes exist without clear accountability.

This is not separate from the larger conversation happening throughout the conference, it is part of it. As the field continues to evolve through artificial intelligence, early detection tools, and new therapeutic pathways — the question is not just what is possible. It is how those possibilities are being implemented and whether the systems surrounding them are strong enough to support the patients they are meant to serve.

What Happens Before Diagnosis

As those final presentations moved from delayed diagnosis to early detection, and then into comorbidities, another layer quietly sat beneath. One that wasn’t always centered, but was impossible to ignore. When you look at those timelines — years of being dismissed, multiple physicians, symptoms starting in adolescence and going unrecognized — you’re not just looking at delayed care. You’re looking at repeated irreversible psychological exposure.

Chronic pain without validation. Symptoms without explanation. Experiences that are minimized, redirected, or misunderstood. Over time, that does something.

The data supports it, but more importantly, so do the patterns. Across multiple studies and discussions throughout the conference, the timeline in published data varies from 7 to 10 years or 6 to 12 years to a diagnosis on average. Oftentimes involving multiple providers before a patient is ever given an answer. In many cases, that path includes misdiagnoses that range far outside gynecology entirely, sending patients through cycles of treatment that never address the underlying condition.

What fills that time is rarely measured. The loss of stability, the erosion of trust, the constant recalibration of what pain is “supposed” to feel or look like. There were acknowledgments of this woven into conversations on comorbidities and outcomes — depression, low mood, cognitive strain, increased substance use. Not as isolated conditions, but as patterns that follow prolonged disease progression and delayed intervention.

Even the concept of what some are now calling “endometriosis brain” began to surface. Not as a dismissal, but as an attempt to name what patients have been describing for years — memory disruption, executive dysfunction, cognitive fatigue. Changes that are increasingly being linked to chronic inflammation, sustained stress responses, and neurological impact. This is not just about where lesions are found. It’s about what happens when a disease is allowed to persist — biologically, systemically, and psychologically — without being fully recognized.

The conversations around adolescents made that even more clear. Early symptoms are often written off. Pain normalized. Concerns redirected. By the time answers are found, the impact has already extended far beyond the original presentation. Sitting there, watching those final slides, it became clear that this was never just about detection or intervention.

It was about what happens in the space patients show up before either of those things occur. What made that moment even harder to ignore was that these weren’t just themes being discussed from the front of the room. They were the same patterns I had presented within it.

Through my own poster work those psychological and social impacts weren’t theoretical, they were measurable. Advocacy-led community data showed what happens when delayed diagnosis and systemic misunderstanding extend beyond the clinical setting and into everyday life. Work disruption, academic penalties, strained relationships, and identity shifts that don’t get captured in traditional medical frameworks, but shape outcomes just as much as any surgical finding.

Across a global dataset, the diagnostic delay echoed what was being presented clinically. But what stood out most wasn’t the timeline itself, it was everything that filled it. At the same time, the “Lived Experiences of Endometriosis Traveling Art Exhibition” I curate brought another dimension into the space. Translating patient narratives into visual and thematic data revealed patterns that extend beyond symptoms alone. Through emotional expression, language, and recurring markers of dismissal, delay, and adaptation. The kind of data that doesn’t just tell us what the disease is doing physically, but how it is being experienced in real time.

In many ways, this is where the conversation begins to come full circle. Not back to definitions, but to experience. If artificial intelligence is going to play a role in earlier detection, then the data it learns from matters. Not just clinical imaging or surgical findings, but lived experience itself.

The way symptoms are described.
The way patients communicate distress.
The way delay presents long before a diagnosis is ever made.

So while the conference returned to early detection as a clinical priority, there was a parallel conversation happening. One that asked whether we are ready to include the full scope of data required to actually make change possible.

Coming Full Circle

By the time my clinical puzzle reappeared on the final day, the weight from the start had definitely shifted. What started as a quiet recognition became something much harder to ignore. Those slides of mine shown were never just about definitions. They were about tension. About uncertainty. About the space between what we think we know and what we are still trying to understand.

Those slides carried more than information. They carried years of lived experience, research, and questions that patients have been asking long before they ever reached conference halls. Yet, even in a room built around progress, there was still that familiar edge — the feeling of being close enough to the conversation to see it clearly, but not always close enough to fully shape it.

The puzzle was there. The questions were there. The tension was there. But mention of it being my work was missing. Sometimes the room still moves forward before patients are given the space to finish or even introduce the thought. That feeling was not new.

Many patients know it well — the experience of recognizing your own body in the discussion while also feeling the distance between being referenced and being fully heard. Advocacy often lives in that space. You are invited to contribute, but still fighting to prove your expertise belongs there, to be recognized. Not because the science is separate from lived experience, but because too often the system still treats them as if they are.

After three days of conversations, innovation, debate, and reflection, those questions were still there. Not as a failure, but as a reminder — a reminder that endometriosis does not present as a single story. That even within the same diagnosis, lived experience can look completely different from one person to the next, shaped by biology, timing, access to care, comorbidities, and the systems meant to respond to it.

By the end of the conference, that puzzle had been acknowledged from multiple angles. It was no longer a question of whether it existed. Discussions around delayed diagnosis, disease progression, systemic involvement, and surgical complexity reinforced how much of this disease extends beyond any one definition or framework. But recognition alone did not resolve the tension. Understanding complexity and fully integrating it into care are not the same thing.

That is where the concept of the clinical puzzle returns — not just as a visual or a moment, but as a framework. One that asks us to consider what it means when the same diagnosis presents in fundamentally different ways across patients. When biology, symptom expression, progression, and impact refuse to follow a single pattern. When variation is not the exception, but the rule.

Yet that is often where the conversation pauses.

What I saw reflected back in those final day slides was not just alignment. It was a continued distance — a space between what is being observed, how it is is being defined, and how it is ultimately acted on. Between lived complexity and the systems still trying to contain it. Between progress being discussed and progress being fully realized.

What stayed with me most was not frustration, but clarity. If we are serious about advancing this field, patient voices cannot remain symbolic additions to the conversation. They have to be part of the architecture. Not only as stories after the fact, but in the design of the questions themselves.

Because sometimes the most important thing in the room is not the answer. It is who is allowed to ask the question. So while the room acknowledged uncertainty, evolution, and the need for continued exploration, the question that remained was not whether the puzzle exists — it was whether we are willing to follow it all the way through.

The puzzle was never the problem alone. It was what we chose to see within it.

Where This Leaves Us

AGCES 2026 was filled with brilliance, progress and with people who are pushing this field forward in real and meaningful ways. Yet moments of stagnation were still present, which made something very clear. We are still in the middle of defining this disease. We are in the process of understanding its biology, and navigating how to diagnose it earlier. Still balancing innovation with caution while still learning how to truly center the people living with it.

Perhaps most importantly, still deciding what we are willing to question or even acknowledge. Progress is happening. There is no denying that or stopping it. But progress without clarity risks carrying the same limitations forward into more advanced systems. Innovation, no matter how promising, does not replace the need for accuracy, accountability, and access.

What this conference ultimately revealed is not a field that is falling behind. It is a field actively in transition, moving through what will be considered the markings of history. A field that is beginning to confront its own assumptions. One that is expanding its tools faster than its definitions. One that is starting to listen, but has not yet fully integrated what it is hearing.

Sometimes, the work that helps move that process forward is already in the room. Even when it is not named.

There was a moment, standing in a hospital room before yet another surgery, when I remember thinking with complete clarity…

“If I do not survive this, people still will not understand what happened here.”

That thought did not come from fear alone. It came from years of dismissal. From the weight of being repeatedly told that pain this severe was normal. From watching my body fail in ways no one could explain while still being expected to function like nothing was wrong. From realizing that even in the moments when medicine becomes most serious — operating rooms, consent forms, anesthesia, life-altering decisions — you are often still fighting to be believed.

People often ask how I ended up here—working between policy meetings, research posters, congressional language requests, art exhibitions, national advocacy efforts, and building frameworks around healthcare reform. The truth is, I did not choose this work. I survived it first.

For over sixteen years, I lived inside a body no one seemed willing to believe.

Who am I if no one believes me? Who am I when teachers think I’m exaggerating? When I’m passing out in school hallways and the response isn’t concern—it’s doubt? Who am I when employers question my reliability instead of asking if I’m okay? Who am I when my body is screaming, and the world around me keeps saying “You’re fine”?

For years, I lived inside that question. But when you live in that question long enough, it starts to reshape who you believe you are.

Symptoms were minimized. Pain was normalized. Questions were dismissed.

Like so many others with endometriosis, I was told it was stress, hormones, anxiety, relationship problems, bad periods, or simply something I should learn to tolerate. I learned early how quickly medicine can reduce a person to inconvenience when their symptoms do not fit neatly into a system built on outdated assumptions.

There is a quote that has stayed with me through all of this…

It is centuries old, and somehow still painfully relevant. Because if the mind is trained to look for the wrong thing, it can look directly at the truth and still miss it. That is exactly what happened to me. When medicine reduces women’s pain, it does not just misdiagnose disease. It delays scientific progress.

My first surgery lasted thirty-five minutes.

When I woke up, my ears were ringing — that strange underwater feeling when anesthesia has not fully left your body. The room was quiet. Too quiet. I remember frantically calling for a nurse, trying to get answers, trying to understand what had just happened.

But the responses were vague.
Dismissive.
Detached.

And then he came in. The surgeon.

He did not sit down.
He did not slow down.

He said…

“You’re clean as a whistle.
Work on your diet and mental health.”

Those words did not just land, they stung. Because in that moment, I felt something inside me shift — like I was being pushed backward through time.

Back to high school where I was passing out and being told it was stress or it was anxiety. That it was all in my head. Back to psychiatric hospitals. Because the pain I felt was not believed. Because my reality did not match their understanding.

Back to the self-harm and suicide attempts. Relationships collapsing under the weight of something no one else could see. Even after surviving domestic violence, I am still living with the physical damage it left behind. A permanent back injury, spinal cord stimulators, and ongoing thoracic pain that became another reminder of what happens when your body is overpowered and your voice is ignored.

So when he told me to “work on my diet and mental health”, it was not just dismissive in that moment. It reopened wounds I had fought to survive. Yet — even in that moment — there was a small voice inside me. A gut feeling, and it did not go away. When I walked away from that surgery, that gut feeling followed me.

Heavy.
Persistent.
Unshakable.

I could not explain it, but I knew something was wrong. So I listened to it. I did what too many patients are forced to do, I researched and searched.
I reached out and connected. I found communities and resources I did not even know existed — people who understood what it felt like to not be believed.

Within one week of that first surgery, I was scheduled with an endometriosis specialist almost two hours away for a second opinion. Within two weeks, I was scheduled for emergency surgery. She personally pushed insurance approval through.

By that point, I was incredibly sick. I had nowhere else to go.
I was on my last straw. But that gut feeling kept me moving.

When I woke up from the second surgery, I did the same thing I had done before. I called for a nurse. But this time, it was different.

She came to my bedside.

She did not rush nor deflect. She held my hand and simply said…

“I’m going to get the doctor.”

When the surgeon came in, she did not stand across the room.

She came right next to me.
She took my hand, and she told me what she found.

Endometriosis had taken over my colon, my rectum, and my bladder. Everything I had felt. Everything I had been told was in my head.

It was real, and in that moment, the weight I had been carrying for years lifted.

To be believed is to be alive. To be seen is to exist. For the first time in a very long time, I felt like I was finally — here.

But diagnosis was never the finish line. It was the beginning of understanding how much had already been taken. By the time endometriosis finally had a name, it had shaped nearly every part of my life — my education, my work, my finances, my relationships, and my trust in the institutions that were supposed to help.

I accumulated medical debt trying to find answers for something I could not even properly label. Debt collectors called while I was still actively in treatment. Bills stacked higher while specialists contradicted one another and basic care remained inaccessible.

The disease itself was never limited to what medicine wanted to call “reproductive.”

It was full-body.
Systemic.
Inflammatory.

It affected my GI system, bladder, pelvic floor, musculoskeletal health, fatigue, cognition, and daily function. It shaped how I parented, how I worked, slept, and ow I moved through the world. It changed what basic survival looked like.

At the same time, I was navigating pelvic floor therapy, pain management, bladder instillations, Botox injections, procedures, imaging, and now rheumatology conversations around autoimmune concerns.

Later coming across the diagnosis of Ehlers-Danlos Syndrome — another confirmation that what I had been feeling was real and interconnected. Another gut feeling, that something else wasn’t quite right and there was more to this picture. Another reminder that too often, patients are left to connect the dots themselves.

Then came surgery again. This marked 8 surgeries in 7 years. Third related to removal of endometriosis. The other five were complications from the previous disease presence and other comorbidities.

This was not local, not easy, and not extremely accessible. I had to travel across the country for specialized excision surgery, from one of the best in the world, because the previous surgeon who diagnosed me admitted to my newer issues becoming too complex for her skills. I was dropped as a patient. Proximity to gynecologic surgeons does not equal expertise, and too many patients are forced to become investigators, fundraisers, case managers, and advocates just to access competent care.

Being dropped for being complex meant surgery could be higher risk. It meant anesthesia issues with a new team if other protocols are not followed, as I have had issues that took a while to get a hold of. New team members after years with a team I connected with because they saved me. It meant sitting in that hospital room carrying the full weight of what happens when your life depends on systems that have already failed you for years.

That moment changed me, yet again. The growing we do as we navigate this trauma is insane. No one should ever have to navigate this. When you are staring at anesthesia forms and risk paperwork, wondering whether your children will remember you, or if the risks outweigh the benefits in a surgeons hands….the conversation around “awareness” starts to feel painfully insufficient.

Awareness is not enough. Not when people are dying unheard. When patients are being handed medications built on falsified data, or being put on unregulated compounded medications, or experiencing years of dismissal instead of proper treatment. Not when debt collectors are louder than physicians.

I am now 8 months post-operative as this is published, still navigating recovery, still managing the financial aftermath, and still watching how often patients are expected to carry systems that continue to fail them.

That reality built my work. I stopped asking how to survive quietly and started asking why so many of us are forced to. That question became the foundation of everything I do now.

I started Getting the Better of Endometriosis first as survival after being diagnosed in 2018, then as advocacy, and eventually as an educational and policy-driven organization built around systemic reform where mother and husband joined my board. This was about family survival too. I have begun to secure my work and shift Getting the Better of Endometriosis as an LLC business. More ways to support my other work and more collaboration opportunity.

Through Worldwide EndoMarch, I serve as a Research Assistant and Colorado Representative helping build national efforts around education, outreach, and patient-led evidence.

Through the American End of Endo Project, I became part of congressional outreach efforts that helped advance 2026 federal appropriations language recognizing historically, endometriosis as a chronic, systemic inflammatory disease—not a narrowly defined reproductive condition. We now host online and in-person advocacy workshops teaching others how we did.

That language matters. Because research follows definitions, and definitions determines who gets believed.

Alongside three other women — with no pharmaceutical funding, no lobbyists, and no institutional power — we helped move federal language. Four regular people walked into congressional offices asking for change. We proved patient voices can move policy. Because experience is not separate from expertise, it is expertise.

At the same time, I became CEO of SATIREV Projects, helping lead international art, literature, and research initiatives including Project 514-415 and the Traveling Lived Experiences of Endometriosis Art Gallery.

Through exhibitions, published collections through Amazon, workshops, and collaborative research, we transformed lived experience into evidence. Art became one of the most powerful tools in that work. A gallery wall can make people understand in five minutes what years of clinical language fails to communicate. Through visual storytelling, we created space for people to see the disease beyond the textbook — through fertility loss, delayed diagnosis, invisible disability, grief, isolation, survival, and resilience.

That work expanded into collaborations with advocacy organizations, journalism, public speaking, and national education efforts where storytelling, policy, and reform became part of the same mission. I have now joined FLARE as lead in Advocacy and Voice lending my support in collaboration, insight and creative strategies.

Because when we share lived experience, we do more than raise awareness. We expose systems, challenge stigma and create evidence. Force institutions to answer for what they have normalized. But I realized quickly that awareness alone was never enough. We needed structure, language, a framework.

That is where B.R.I.D.G.E. was born. B.R.I.D.G.E. is the foundation of my work.

Believe.
Record.
Integrate.
Design.
Generate.
Elevate.

Believe lived experience first — because if we do not believe patients, we build systems on sand.

Record stories honestly through art, literature, and data — because anecdotes become patterns when we listen collectively.

Integrate lived experience into research, education, and policy — not as an afterthought, but as legitimate evidence.

Design systems that reflect biological reality, not outdated theory.

Generate measurable change through funding language, clinical shifts, and structural reform.

Elevate the next generation so justice becomes standard, not revolutionary.

This framework is not theory to me. It is survival translated into strategy. It is what happens when pain becomes policy, when grief becomes structure, and when being dismissed for long enough teaches you how to build something stronger than permission. It is why I no longer ask for a seat at the table.

I build new tables.

Because meaningful change happens when lived experience is recognized for what it has always been, expertise.