A gynecologist hearing a patient’s symptom of painful sex might explore a range of causes—from a sexually transmitted disease to menopause, with a different set of treatments for every possible cause along the way. And for back pain, you’re likely to be prescribed painkillers until the pain finally sends you to an orthopedist, who might recommend physical therapy for the back or even suggest surgery. Yet endo can encompass all of these separate conditions—and more—and you might undergo a series of interventions and take a range of prescriptions, month after month, year after year—to little avail.
That is typically what happens during those nearly twelve years between the onset of endo symptoms and its proper diagnosis. Twelve years is a long time to be in pain or discomfort, and it is a long time to be without an answer, without a plan of action, and without hope of a resolution. Why is this disease so difficult to diagnose? How does it happen in the first place? Why does it miss most women yet hit some women so very hard?
The truth is, when it comes to endo, the medical community has more questions than it has answers. But the one thing we are pretty certain of is that the lesions Iris finds when she operates on endo patients are the pathological consequences of that disease process that is set in motion when cells similar to those of the uterine lining grow outside the uterus. Since they’re not supposed to be there, this prompts an inflammatory response, more or less the way any anomaly—an injury or an infection—prompts such a response as a defense mechanism. It’s a little like what happens when you scratch your skin with a fingernail; whatever your pigment, the color of the skin at the spot you scratched turns a different shade. That’s basic; it’s Biology 101.
We also know what happens when cells form in the uterine lining because it happens on a cyclical basis, as all women are reminded once a month. Your ovary releases an egg and sends it toward the fallopian tubes. Hormones stimulate the uterus to thicken its lining in anticipation of the possibility of fertilization. But when sperm fail to fertilize the egg, the egg simply dissolves, and the uterine lining, along with some blood, flows out of the body—i.e., you get your period. All of this too is basic. It’s Procreation 101—how the species keeps going—and most women’s bodies are equipped to undergo this chance at fertilization every twenty-eight days or so, year after year from the time of our first period as a young girl until we age into menopause (except during pregnancy, of course).
The cells that are found outside the uterus are also stimulated each month by the same hormonal cycle. But these cells have nowhere to go; there is no exit point for them, so they get thicker and thicker month after month. In time, they distort the surrounding anatomy, and this can cause the organs in the area to stick to one another—the rectum to the uterus, for example. In women in whose bodies this process is taking place, the mechanism for clearing out the cells has altered in some way and fails to work. The cells accumulate, month by month, year by year.
Nor are endo implants limited to the vicinity of the reproductive organs. They can be anywhere—the lungs, the diaphragm, anywhere. Iris knew of a patient who suffered nosebleeds at every period; her endo implants literally were in her nose.
While we don’t know exactly why these cells grow outside of the uterus, research suggests that there are both genetic and environmental factors that can put a woman at increased risk of developing the disease. If your mother, sibling, aunt, or grandmother—via either the maternal or the paternal line—has or had endometriosis, you have a sevenfold to tenfold greater chance of developing endo than the rest of the female population. That’s the genetic factor in spades.
Other research, in the form of fetal autopsy studies, shows that an estimated 9 percent of female fetuses have endometriosis.3 The suspicion of the scientists who performed this research is that either the fetuses inherited the endo cells from their mothers (the genetic factor) or that the fetuses were exposed in utero to a family of chemicals called dioxins (this is the environmental factor). Dioxins are highly toxic compounds found both in the food chain and in by-products of household and gardening or “lawn care” products, and they have long been identified as a cause of endometriosis. If a mother is exposed to dioxins while pregnant, her fetus is exposed to their damaging effects as well.
Meanwhile, the process continues. The consistently thickening endo cells take on a life of their own. They need blood to grow, so they keep on increasing their blood supply. They also go deeper as they grow, and as Iris explains it to patients, they act like Velcro, adhering to whatever is adjacent: the bowel, the bladder, the ovaries, the fallopian tubes. And since each monthly hormonal stimulation continues to fuel endo’s growth and expansion, there’s no stopping the process until a surgeon like Iris excises the endometriosis that is now thoroughly implanted in the body.
Given the average twelve-year period between onset of symptoms and diagnosis, consider the potential extent and severity of your endo by the time you receive that diagnosis. If your endo originated during fetal life, those implants have been growing inside you for a long, long time, during which your body kept on adjusting to their presence. Maybe when you began to menstruate, your cramps were so painful that you had to visit the school nurse’s office and ask to lie down—the likely onset of symptoms. If that set you apart from most of the other girls in your class—and made the school nurse suspect you of being overly dramatic—you probably still didn’t suspect anything wrong, especially if your mother told you she suffered similarly agonizing cramps and said it was just “something we have to put up with.” So perhaps it wasn’t until as a young woman you confronted pelvic pain, or pain during sex, or infertility, that you began to seek “serious” medical attention. By that time, the endo implants had been growing inside you maybe for a couple of decades, initiating symptoms that appeared to different specialists at different times as different conditions. Undoing the impact of the disease at this point would be no small undertaking.
And it isn’t just the implants themselves that cause harm. It is their impact, multiplied as they grow and expand over time, on the central nervous system. As the thickening implants gain increased blood supply, their nerve density also bulks up. More nerves means more sensory messages being transmitted to the central nervous system. More messages being sent trigger more receptors to respond, further sensitizing the nervous system. Each response sends out its own message of stimulus, so there are now more nerves sending more sensory messages. This process essentially becomes a self-sustaining feedback loop in which the number of messages and responses continues to increase, and the scope of sensation continues to expand. The medical term for this “loop” is called upregulation—a process of stimulus and response that just keeps amplifying.
In due course, nerves carrying these sensations of pain overwhelm the central nervous system, which eventually becomes so upregulated that it hits an overload alert. And since those overload messages have to go somewhere, they branch out via the spinal cord to other available pathways. What started as the irritation of a single organ in one part of your body now spreads to other organs, muscles, and nerves in any number of locations. In other words, what starts as a small trigger can result in maximum perceived pain. Physical therapists like Amy are very familiar with the impact of this cross-organ sensitization. They know all about the effects of what they call “viscero-somatic and somato-visceral cross-talk”—organ-to-body and body-to-organ “conversation”—when muscles react reflexively to some ailment or disease condition that starts in one area of the body and moves to others.
The result of this cross-talk and of all the physiological changes brought about by the inflammatory process is what we call the co-conditions of endo—all too often, a cascade of coexisting conditions: interstitial cystitis/painful bladder syndrome, muscular pain radiating outward and upward and downward from the pelvic area causing pelvic floor dysfunction, gastrointestinal ailments leading to a likely diagnosis of irritable bowel syndrome or small intestinal bacterial overgrowth (SIBO) or both, a revved-up central nervous system—until the whole body feels as if it is on fire.
While the expansiveness of endo can feel debilitating for patients and can be confounding for doctors, the reality is that the way this disease manifests itself makes perfect sense. After all, the body is an interconnected network. Our medical system is divided into separate areas of study and treatment, and so we speak of separate organ systems, but that is just the expedience of jargon; of course there are no