Ask Me About My Uterus Read online

  I went full skeptical Scully on my body, coming up with every reason that it wasn’t that pain. It was just a passing feeling, surely. It wouldn’t last. There was no enduring mystery, no shadow stalking me, no conspiracy. My body was not frantically destroying itself in service to corporeal paranoia, in the form of some kind of weaponized autoimmunity.

  My body was not an X-File. I would still get to go back to Sarah Lawrence. I would get better. This pain would end.

  Not unlike my fictional heroes, I was about to become embroiled in a search for a truth that many did not believe was out there to be found. Like Mulder, I wanted to believe. But unlike Mulder, and more like Scully, what I wanted to believe in was science. I’d had one of Scully’s quotes pinned to the inside of my locker in high school. It had gone with me to New York and back again, and it came to me that afternoon on Cass’s couch: “Nothing happens in contradiction to nature, only in contradiction to what we know of it. And that’s a place to start. That’s where the hope is.”

  THE PREEMINENT RESEARCH ON ENDOMETRIOSIS started in the 1980s, led by an esteemed surgeon named Dr. David Redwine. Shortly before his retirement in 2012, he gave a presentation on the subject at the Endometriosis Foundation of America’s annual medical conference (which I would later speak at myself). I didn’t know much about him or his work, but I liked that he talked about astronomy in his speech: his title was “Asteroid Mapping, HOX Genes and Endometriosis.”

  Redwine likened the mapping of constellations in the night sky to his development of a way to map the pelvis in order to identify locations where endometriosis may be likely to occur. He developed the pelvic mapping based on the thousands of surgeries he performed on women with “endo,” and he continued to question the veracity of the prevailing theory by gynecologist John Sampson, which was developed in the 1920s. “Sampson’s theory,” as it is called, purported that menstrual effluent could essentially “backwash” from the uterus, through the fallopian tubes, and out into the pelvis, where it would then implant itself as endometriosis. The rupture of a blood-filled endometrioma—or cyst, like the one I had—would have a similar capacity, according to his theory. Although the theory was presented nearly a century ago, it’s never been irrefutably proven, despite the advances of medical technology that would arguably make it possible to do so, if there were substantial interest and investment.

  Despite the passage of time and the ensuing progression of medical science, neither are medical textbooks overflowing with high-definition imagery of endometriosis. Although Redwine and others have pointed out that research regarding endometriosis has been happening for at least the past century, every medical textbook I’ve ever thumbed through (hundreds, at various hospitals, libraries, and medical centers around the United States) seems to demarcate the condition as being relatively uninteresting: even in textbooks entirely devoted to reproductive endocrinology or gynecologic surgery, the passages on endometriosis are short. They usually contain the same refrain about how endometriosis is a disease of the female reproductive system where cells from inside the uterus wind up in places that they shouldn’t. Infertility is usually the bolded point of interest. The litany of facts presented, even in the more contemporary texts I’ve read, sometimes seem bloated to me. These passages can read like college term papers written the night before they’re due, wherein a lot of unnecessary words are added to make the paper longer.

  You’d think that after reading thousands of pages about endometriosis I’d feel like I know a lot. But I don’t. I feel like I know the same facts and theories very well, but I have been left with an abundance of questions. Some of which are questions that science and medicine appear to be interested in, even if just for the sake of academic conference discourse: Have women always been vulnerable to endometriosis? Were cavewomen staggering around in pain? Can disciplines like anthropology and archeology give us insight? Were those Victorian hysterics suffering from adhesions and cysts? If history had been told by women, would we not be so in the dark about a disease that has, theoretically, always existed? Is the mechanism of disease a product of menstruation? Or is something else key to its development? Does it matter where you’re born and raised, or where your family moved when you were a teen? Is it even possible to unspool all the factors, like genetics, environment, and diet, that influence our state of health in general, let alone the influence it may have on one specific condition? Is endometriosis preventable? Inevitable?

  To whom can we look for answers? Whom can we trust? Our doctors? Doctors writing on the Internet? Doctors speaking at conferences, like Redwine? Or perhaps we can trust the researchers cited in those talks, and the alphabet soup of sources appearing in medical journals. How do I, as a patient, know what to believe, what to build my life upon with this disease? As a young woman writing this book, which can never be comprehensive and is merely trying to put my own experience into context, how am I to know if the information I’ve relied upon in my quest for answers is the “right” information?

  We don’t know much about endometriosis. If you compare what we know about other diseases that affect around the same number of people as endometriosis (such as liver disease), you find that the amount of information we don’t know is startling. If you put “endometriosis” into PubMed, you get about 1,800 pages of results. Liver disease returns over 30,000.

  The scientific and medical establishment doesn’t know much about endometriosis—really, it’s the patients who tend to have their pulses on the most current research. Although sometimes that backfires. A patient’s main motivation for becoming an expert in his or her condition is to manage it—perhaps even cure it. The patient isn’t trying to subvert his or her physician. But a frantic patient who has brought in a heap of research is often chastised, and usually advised to refrain from consulting Google. In the case of endometriosis, it’s shortsighted to cast aside the engaged and eager patient: What physician has the time to review all the current literature on a particular condition? A patient who is trying take an active role in her care will use whatever tools she has available to her within the limitations of her life, limitations that are often determined largely by her disease, her socioeconomic circumstances, and her level of education.

  The patient who brings in a binder full of PubMed articles should be considered not so much for the specifics of what she has found, but for the fact that she has devoted so much time to the search. It may not be that the research she has brought is pertinent, or, at that particular time, even useful. But the very act of researching, and of supplying the fruits of that quest, is clinically relevant, if only because they are evidence of how the condition has affected the patient’s life. I say this as a patient who researched as though my life depended on it. Which I suppose it did. Had the physicians who tutted at my eagerness, at my intellectual intensity, at my DIY medical school education, read between the lines, they would have seen the stacks of medical textbooks next to my bed, and the hundreds of bookmarked articles with up-to-date information, as a symptom of the anxiety that endometriosis caused me. I wasn’t just seeking answers to absolve the pain; I was trying to soothe the fears that stemmed from the uncertainty of it.

  I’m certain that not every endometriosis patient, or every chronically ill patient, for that matter, presents this way. I’m certain that not every patient cares about the whys or hows or what fors. Not every patient will be thrown into an existential crisis trying to find answers to the mysteries of their own bodies. Those who do, like me, are trying to process their physical experience in an intellectual manner. For me, it was in part because I was afraid of fully embodying what it meant to feel unwell. To feel pain. I focused on unraveling the scientific basis of my situation so that I could feel detached from it. I was also seeking answers and trying to give meaning to my suffering.

  I was also, I think, trying to assuage my guilt. As much as I was looking for a reason, or a treatment, or a cure, I was also looking for proof that the disease was purely physical, and not some kind of
cosmic punishment. I needed concrete evidence of rogue cells, of inflammation, of scars and blood and twisted fascia. I needed to understand, fully, the science of inflammation. I clung to the concepts of cytokines, telocytes, interleukins, and genetic polymorphisms because, if I could make them complicit, I could exonerate myself. Blame had been circling me since I had gotten sick, waiting for me to pause long enough for it to devour me. I’d come to feel, deep down in that tangled mess of organs, that the disease was my fault. And no matter how much I searched for evidence to the contrary, it didn’t seem like medicine could entirely prove me wrong. In fact, a lot of people in my life—doctors, psychologists, others—left me feeling responsible. I was frigid, tense, too stressed, too smart for my own good, didn’t have enough fun. Was I searching for an identity in disease? Trying to avoid sex? Fearful of intimacy? Desperate for attention?

  I had no way to defend myself, really. I didn’t think endometriosis was truly a mysterious disease for which there were no answers; science just wasn’t there yet. And until science got there, I would have to endure the doubt. Doubt being a comorbidity with a symptom profile and treatment protocol, a prognosis all its own.

  We don’t know, with any degree of certainty, how or why endometriosis begins. We don’t know why some women get it and others do not. We don’t know why some women get it, suffer, and then appear to stop suffering at certain points in their lives. We don’t know why a woman with only a few scattered lesions might have debilitating symptoms and a woman who is chock-full of them might feel fine.

  Even the textbook facts are not widely agreed upon. The doctor you see, his or her level of experience, and to some extent gender, will determine how endometriosis is explained to you. Some will tell you there’s no cure. Some will say there is a cure, but they can’t provide it. There are plenty of surgeons who could be staring right at endometrial lesions and would not recognize them. There are a few surgeons who are experienced in excising the lesions, and some women have felt that after that procedure, they’ve been cured. Some women who had the touted curative surgery did not feel cured—either because the disease came back, or because some of the lesions were missed the first time around. (According to Dr. Redwine, the research indicates that the cure rate for excision surgeries is around 56 to 66 percent.)

  Not every patient has access to excision surgery. I, for one, was never offered it, and it was only through discussions with other patients that I learned about it. I also learned that the surgeons who did it had very long wait lists and didn’t take my insurance. If excision surgery is, as a matter of scientific fact, curative, what does it matter to me if I can’t access it? And what if that fact doesn’t help me? Do I need permission to push beyond the realm of present scientific fact and look for other possibilities that are within my reach? Is it appropriate, or valuable, for me to assert that possibilities might well exist within my body, or my mind, and that those stagnant facts in perennially outdated textbooks aren’t helpful to me? That they may not be very helpful to a lot of people with this disease? Many of whom are never given “the facts” in the first place?

  Doctors who are not surgeons—or endometriosis-familiar surgeons—often discuss endometriosis as though it were incidental. They might offer birth control, a course or two of Lupron, or simply advise a patient to get pregnant: both because they believe, incorrectly, that pregnancy is curative, and because they think endometriosis is a fast-track to infertility. Some will say that a complete hysterectomy is the only option—not unlike those nineteenth-century physicians who saw castration as the cure-all for their hysteric patients. I suspect that many doctors confronted with a patient who ultimately has endometriosis say, and do, nothing at all—simply because a diagnosis of endometriosis just isn’t on their radar. When you consider that many physicians practicing today, who received the bulk of their medical education prior to the 1980s, only saw endometriosis as a footnote in a textbook, I don’t think we should be that surprised.

  A lot of commonly held beliefs about endometriosis, by the medical profession and the general public, are based in half-truths, or in ideas that were once regarded as true, but were later proved to be false, or at least mostly false, or probably false. Such as the idea that endometriosis lesions come from inside the uterus, and that they are made of the same sort of tissue that lines the womb. And the idea that this tissue is expelled out of the fallopian tubes and into the pelvic cavity, where it implants and causes a ruckus.

  The idea that they are the same sort of tissue is sort of true, according to one popular theory. The problem is that these lesions are not identical to what is found inside the uterus. As Dr. Redwine pointed out in his lecture, endometriosis lesions are not “autografts,” which just means that they aren’t identical to the tissue from which they came. Under a microscope, endometriosis lesions can be inspected and seen to be stromal cells, and yes, stromal cells are also found in the lining of the uterus. But these same sorts of lesions have been found in other places—such as the liver, lungs, and diaphragm—which implies that there is another mechanism of movement that determines how they get there.

  I, for one, have often wondered whether the curious neck and shoulder pain I get during the first few days of my period could be related to endo somehow. I’d assumed that any musculoskeletal pain during my cycle was hormone related, which is a fairly well-documented phenomenon even in people who don’t have endometriosis. But many a Google search turned up discussion forums where others described the same cyclic neck and shoulder pain, only to find out it was related to endometriosis of the diaphragm.

  Now, unless your fallopian tubes are shooting out uterine tissue like a pressure washer, how else could you possibly develop lesions in such remote locations? How do you explain women who have endometrial lesions on their brain, or the backs of their eyeballs?

  The theory that uterine tissue can sort of seep out of your fallopian tubes and end up in places it doesn’t belong is called retrograde menstruation. And, in fact, pretty much anyone who has ever menstruated has probably had some of this menstrual backwash before. What usually happens is that your body recognizes that the tissue doesn’t belong, and wipes it up. Your immune system should respond to that uterine tissue in your pelvic cavity like, “What is this mess? Really? I let you live here rent-free and you can’t even pick up after yourself? How hard is it to keep the mess contained to your own damn space. Honest to God,…” so muttering as it reluctantly mops up the mess.

  The human immune system is like the TV sitcom mom of yore who begrudgingly cleans up the messes of the rest of the family. So when an autoimmune disease occurs, it’s kind of like your internal immune-mother goes full Thelma and Louise and bails on you without so much as a casserole in the freezer.

  Researchers are curious about what, if any, interplay exists between endometriosis and the autoimmune system. Is endometriosis something that occurs because of a compromised autoimmune system, or does the presence of endometriosis lead to autoimmune dysfunction?

  The link between endometriosis and fertility, meanwhile, is less about causation and more about correlation. Endometriosis is more likely to be diagnosed in women who are infertile because those women are seeking treatment since they can’t get pregnant. This doesn’t mean that women with endometriosis are doomed to infertility, and in fact, recent cohort studies see a much smaller correlation than is typically espoused. Endometriosis—particularly advanced stage disease in women who have never undergone any kind of surgical treatment—could certainly contribute to infertility structurally. But many women with endometriosis are able to get pregnant and go on to have normal, uncomplicated births.

  The current model of staging endometriosis is often criticized because it has an arbitrary point system for classification, which is fantastically short-sighted when you consider that the disease can cause such debilitating symptoms. Staging other chronic diseases, such as multiple sclerosis, factors in not only test results but also quality-of-life indicators or episodes of s
ymptoms. Flare-ups of multiple sclerosis can take on different timetables, too—being “relapsing-remitting,” in some cases. Could endometriosis, a hormone-dependent disease, at least at the outset, also be capable of appearing on a relapsing-remitting course?

  Symptoms of endometriosis can persist throughout the month, but the majority of women I’ve interviewed agree that the flow of symptoms is at least influenced, if not driven, by their menstrual cycle. Because of the tissue’s similarities to uterine tissue, research has posited it’s estrogen-dependent. Treatments that aim to suppress estrogen sometimes provide relief, but for some, when that treatment is discontinued the symptoms return. Similarly, many women find relief from their pain during pregnancy, but once the baby is born, the normal pattern of symptoms resumes.

  Who are we talking about here? Who gets endometriosis? Do we even know? Some studies cite an incidence of as little as 2 percent of the general population, others of as much as 10 percent. Although the most commonly touted figure is “one in ten women,” one should always refer back to the population being studied to produce that statistic. Many of these studies obtained their data by reviewing medical records for things like surgeries and hospital stays—which means the women included in their cohort are only those who had access to health care. Access to health care varies not just state to state, but even within states, and even within communities.

  When studies conclude that endometriosis is a disease predominantly seen in white women, we need to be very critical of that assessment: just because the women whose hospital records were reviewed were predominantly white, that doesn’t necessarily prove that more white women have endometriosis. What it tells us is that more white women are accessing health-care services. Poor women, minority women, LGBTQ persons, and people with mental or physical disabilities face significant challenges accessing health care even at the most basic level, such as for an annual physical, let alone specialists for problems like endometriosis or infertility.