The Conversation About Endometriosis Has Changed. Here Is What That Means For You.
Reviewed Dr Jo Mackson, MBBS FRACGP
Published August 2026
Reading time 40 to 45 mins, 5 to 6 mins per part
Short on time? Start with the Mini Guide, then come back here when you want the full picture.
Before we begin our deep dive into endometriosis, we need to acknowledge why you are reading this in the first place.
Women’s health has historically been under-researched, over-simplified and too often dismissed, leaving most of us trying to make sense of our own bodies without the education we need to do so. That is why this Deep Dive exists. Because as women, most of us have never been taught the specific biology that shapes so much of our lives. School sex ed for most of us was a brief tour of the fallopian tubes, an introduction to pads and tampons, and the unforgettable awkwardness of a condom on a banana. Our mothers, aunties, and grandmothers were often taught even less, resulting in a knowledge gap that has been quietly handed down for generations. This stops here.
So bear with us if this Deep Dive gets a bit science-heavy, and we apologise in advance for any flashbacks to the Year 8 science lab. We promise it will be worth it, because we believe knowing the science that underpins your life as a woman is far more useful than knowing how plants turn sunlight into food. Unless you are a botanist.
Because once you understand the why, everything that follows, the symptoms, the investigations, the treatment options, starts to make sense.
So yes, there will be medical terminology, the odd graph, and drug names that look like a toddler was let loose on a keyboard. Read it at your own pace. Skip ahead if you need to. Come back to the parts that matter most for you. Consider this the education that is long overdue. And don’t worry, there is no pop quiz at the end. Although if retrograde menstruation comes up at your next trivia night, you can thank us later.
Now, before we let you loose below, a quick note about that medical terminology. If you are reading online, just toggle your mouse over the word and you can get a brief definition. If you have printed and are reading it old school, hats off. We have included a glossary at the end of the guide just for you.
What Endometriosis Actually Is (And What It Is Not)
The disease itself, not the tidy version.
Endometriosis is a chronic inflammatory disease in which tissue similar to the lining that exists inside your uterus grows in places outside your uterus. Places it is not supposed to be. You may have been told that endometriosis is “the lining of the womb growing outside the womb,” but that explanation is a little oversimplified. Endometriosis tissue is similar to the uterine lining, but it is not identical to it, and the difference is responsible for why endometriosis behaves like an inflammatory condition, not just an anatomical one.
Around 1 in 7 Australian women have been diagnosed with endometriosis by their late forties. That figure comes from the Australian Institute of Health and Welfare, which followed a group of women born in the 1970s through to age 49 and found 14% had received a diagnosis. The number you will see quoted more often is 1 in 9, which is the estimate across all reproductive ages. Either way, it is about as common as asthma. And yet most women have never been given a proper explanation of what is happening in their pelvis. So let’s start there.
Endometriosis is not just a hormonal condition. It is also an inflammatory one.
The lining of your uterus is called the endometrium. It is a hormonally responsive tissue, which means it changes under the influence of your natural hormones, and under the influence of hormonal medications. The endometrium is what allows a pregnancy to implant and grow.
Endometriosis tissue responds to your hormone cycle in much the same way the endometrium does. But it is not just endometrial tissue growing where it shouldn’t. Three things make it its own beast.
First, it produces its own local oestrogen. Your ovaries produce most of the oestrogen in your body, and a small amount comes from fat tissue. Endometriosis lesions make their own, locally, on top of that. In practical terms, the lesions make their own fuel, which is part of why the disease can be stubborn even when treatment is suppressing the ovaries.
Second, it recruits its own blood supply. The lesions grow new blood vessels to feed themselves, which is part of why they can grow, persist, and bleed internally each cycle.
Third, and most importantly, it provokes a strong inflammatory response from the surrounding tissue. The body recognises the lesions as foreign and tries to manage them the way it would manage a wound. But the lesions are not a wound that can heal. They are tissue that is alive, hormonally active, and constantly reactivated by the cycle. So instead of a short inflammatory response like one to heal a cut, you get a low-grade, chronic, smouldering inflammation that does not switch off. Over time, that inflammation contributes to pain, scarring, adhesions, and changes in how nerves in the pelvis function. This is the reason endometriosis can cause pain that does not seem to match the size or location of the visible lesions, and why removing the lesions surgically does not always remove the pain. Inflammation is part of the disease, not just a side effect of it.
Endometriosis can grow almost anywhere in the abdomen and pelvis, but some locations are much more common than others.
The most common sites are the surface of the ovaries, where lesions can form fluid-filled cysts called endometriomas (sometimes called “chocolate cysts” because of the dark old blood they contain); the peritoneum, the thin membrane that lines the abdominal cavity; the ligaments that support the uterus; and the surfaces of the bowel and the bladder.
Less commonly it grows into the muscle of the bowel or bladder wall, which is called deep infiltrating endometriosis, or inside old surgical scars. Rarely, it appears on the diaphragm or in the lungs.
A woman can have lesions in one location, several, or many. The location and how invasive the disease is shape both the symptoms and the treatment options.
How does it get there? The honest answer.
We do not know with certainty. Four theories have been proposed and refined over the past century, and the current view is that endometriosis is probably driven by a combination of them rather than any single mechanism.
The oldest and best known is Sampson’s theory of retrograde menstruation, proposed in 1927. The idea is that during a period, some menstrual blood flows backwards through the fallopian tubes and leaks into the pelvic cavity, carrying endometrial cells with it. Those cells then implant on the peritoneum and grow. This is almost certainly part of the story. Retrograde menstruation is very common (it happens in most women to some degree), but only some women develop endometriosis, which tells us retrograde flow alone is not the whole story.
The second theory, coelomic metaplasia (yes, that is the actual name, and no, you will never need to remember it), proposes that the cells lining the peritoneum can change into endometriosis tissue under the right conditions. This would explain why endometriosis sometimes appears in women without functioning periods.
The third, lymphatic and vascular spread, proposes that endometrial cells can travel through the lymphatic system or bloodstream to distant sites. This is the leading explanation for the rare cases of endometriosis in the lung or diaphragm.
The fourth, stem cell theory, is the newest. Stem cells are cells in the body that can develop into different kinds of tissue. The theory is that some of these cells travel from the bone marrow or from inside the uterus itself, and transform into endometriosis tissue in and on organs far beyond the pelvis.
Which theory is right matters most to researchers, because the answer shapes where they look next. For the woman in front of us, what matters more is that endometriosis is real, the mechanisms are at least partially understood, and the treatment options work.
What endometriosis is not.
There are a few misconceptions of what endo is, that is worth correcting before we go any further.
Endometriosis is not “a bad period.” Period pain that is mild to moderate and resolves with simple measures is common and not a sign of disease. Pain that is severe, that interferes with daily life, that requires you to miss school or work, or that has crept beyond the days of bleeding is different. We will come back to this in Part Two.
Endometriosis is not adenomyosis, although the two are often confused and they frequently coexist. Adenomyosis is endometrial-like tissue growing into the muscular wall of the uterus itself, rather than outside it. The symptoms overlap (heavy bleeding, period pain), the treatments overlap, but the conditions are distinct. We have a separate Deep Dive on adenomyosis coming, and for now the short version is: endometriosis is outside the uterus, adenomyosis is inside the wall of the uterus, and a woman can have either, both, or neither.
A quick refresher on the cycle.
Before we get to how endometriosis causes pain, we need a shared understanding of what your hormones do during a typical cycle. The reason: endometriosis is hormonally responsive, the pain it causes typically tracks with your cycle (at least at first), and the treatment options work largely by changing what your hormones are doing. So if the cycle is fuzzy, the rest of the guide will be too.
The menstrual cycle is the rhythm your hormonal system has run on since puberty: a tightly coordinated conversation between your brain and your ovaries that repeats itself month after month. Endometriosis is, in part, what happens when this conversation happens in tissue in places it was never supposed to be. So before we can understand what is happening, we need to understand the usual rhythm first.
Let me introduce you to the menstrual cycle. Your monthly reminder that we are the ones carrying the human race forward, whether we asked to or not.
The cycle has two halves: a build-up to ovulation called the follicular phase, and a waiting period after ovulation called the luteal phase, when the body holds steady to see whether a pregnancy has occurred.
A less textbook version? Think of the menstrual cycle as preparing a guest room for a notoriously flaky friend. The first half is all preparation. Oestrogen rises, the lining thickens, an egg readies itself for ovulation. You put fresh linen on the bed, plump the pillows, place fresh flowers on the nightstand. The second half is the wait. If she turns up, the room is all ready for her stay (biologically speaking, you’re pregnant). More often than not, she sends a late text and is a no-show. You strip the bed, toss the wilted flowers, and the cycle begins all over again.
Day one of the cycle is the first day of your period. In hormonal terms, this is the body saying: not pregnant this month, time to start again.
Your brain sends a hormonal signal to your ovaries to encourage a group of follicles (each containing an egg) to start growing. These follicles enter a kind of quiet competition. One follicle grows faster than the others and becomes the dominant follicle.
As this dominant follicle grows, it produces oestrogen. One of oestrogen’s jobs is to build up the lining of the uterus, getting it ready in case a pregnancy needs to settle in.
Around the middle of the cycle, once oestrogen has risen high enough, the brain sends a trigger signal telling the dominant follicle it’s show time, time to rupture and release its egg.
And ta da. Ovulation.
After ovulation, the empty follicle does not just disappear. It transforms into a structure called the corpus luteum, kind of like the follicle’s second act.
The corpus luteum sits in the ovary for the next 12 to 14 days and produces progesterone. Progesterone’s job is to keep the uterine lining steady and support an early pregnancy if that was on the menu that month.
If a pregnancy occurs, it implants into the endometrium and starts to make its own progesterone to keep the endometrium nice and thick. However if pregnancy does not occur, the corpus luteum eventually breaks down. Progesterone levels fall. The endometrium becomes unstable and eventually sheds.
Enter: your period. And the cycle begins again.
Now, with all of that in view, let us look at how endometriosis hijacks this natural monthly rhythm and turns it into a source of pain and dysfunction.
How Endometriosis Causes Pain, And Why “Normal” Periods Should Never Be Disabling
Five mechanisms, working together.
Endometriosis causes pain through several mechanisms working together. Understanding these mechanisms matters because they explain things that often confuse women with the disease: why the pain does not always match the appearance of the lesions on a scan, why it can occur outside the days of bleeding, why removing the lesions surgically does not always remove the pain, and why effective treatment usually involves more than one approach.
Endometriosis tissue responds to your hormonal cycle in the same way the lining of your uterus does. It builds up and becomes active under the rise of oestrogen, holds steady under progesterone, and breaks down when both hormones drop at the end of the cycle.
Inside the uterus, that breakdown is your period. Outside the uterus, the same breakdown happens, but in tissue that is not built to manage it. The lesion produces microscopic bleeding into the surrounding tissue, releases the chemicals that drive inflammation, and sheds cells the body has to clear. The immune system responds the way it does to any source of irritation, by mounting an inflammatory response.
This is the pain most women recognise as their typical endometriosis pain. It tracks with the cycle, it gets worse around the period itself, and it improves between cycles. In milder disease, this may be the only kind of pain. In more advanced disease, unfortunately it is one of several.
The inflammation that starts in the lesions does not stay in the lesions. The chemicals that drive it (prostaglandins, cytokines, and other inflammatory signals) diffuse into the surrounding tissue and circulate more widely. The whole pelvic environment becomes inflamed. In more advanced disease, this can extend further still, producing a low-grade inflammatory state that affects the whole body.
This is why endometriosis is rarely just a pain condition. Women often describe a generalised “endo flare” feeling that is not just pain in one specific spot, but a whole-pelvis, and sometimes whole-body, sense of being unwell. Fatigue, brain fog, generalised aching, low mood. These symptoms are part of the inflammatory picture, not signs that the disease is “in your head”.
In more advanced endometriosis, the repeated cycles of inflammation can cause scar tissue and adhesions. Adhesions are bands of fibrous tissue that can stick organs together: the bowel to the uterus, the ovary to the pelvic sidewall, the bladder to the uterus. When organs are stuck rather than free to slide freely, normal every day movements (a full bladder pressing on the uterus, a bowel motion, sex) can cause pain. This is the pain that is most associated with deep infiltrating endometriosis, and it is the kind of pain that does not always track with the cycle: it can be there all month, because it is structural, not hormonal.
Living with chronic pelvic pain, for any reason, often results in the pelvic floor muscles becoming tight and reactive. The pelvic floor is a group of muscles that supports the uterus and surrounds the bladder, the vagina, and the rectum. When these muscles are tight, they cause their own pain (often described as a deep ache, pain with sex, or pain with bowel movements), and they can perpetuate pain even when the underlying endometriosis is being well treated. This is where pelvic floor physiotherapy makes a real difference for women with endometriosis. More on this in Part Five.
Pain that has shaped your life around it is not pain to be managed in silence. It is pain that deserves a name, a workup, and a plan.
This is the one most women have never had explained to them, and it is one of the most important reasons endometriosis pain can become harder to treat over time.
When tissue is chronically inflamed and repeatedly irritated over months and years, the nerves that carry signals from that tissue can change. Think of it like a smoke alarm that has gone off so often that it eventually starts triggering at the smallest hint of smoke, or even when there is none at all. In endometriosis, the nerves in the pelvis, after years of carrying pain signals to the brain, can start firing pain signals at lower and lower thresholds, meaning your body starts interpreting things as painful that it would not have flagged before. A full bladder. A bowel motion. Sex. And it does not stop at the nerves themselves. The spinal cord and brain, which are where the pain signals end up, also adjust and start amplifying the signals coming in. After enough time, the whole system has recalibrated to be on high alert, and it stays that way even after the original irritation has settled. This process is called central sensitisation, and it is well-established in pain medicine as a feature of many chronic pain conditions, not just endometriosis.
The practical consequence is that, in long-standing endometriosis, the nervous system can become so sensitised that it produces pain even when the lesions themselves are being treated or even surgically removed. The pain is real. The signals are real. They are just coming from a nervous system that has been processing pain signals for so long it can no longer tell the difference between active inflammation and the memory of it. This is why pain neuroscience and pelvic floor physiotherapy are crucial parts of endometriosis treatment, not optional extras. We will come back to this in Part Five.
The “normal period” question, answered plainly.
A surprising number of women come to us not sure whether their pain is normal. There are good reasons for that. For generations, society has framed period pain as the price of being a woman. Many of us were raised by mothers and grandmothers who managed their pain in silence, not because they wanted to, but because no one had told them they had any other option. Many of us have been told by a doctor, somewhere along the line, that period pain is a normal consequence of having a uterus. So how do you tell?
The short version: pain that is mild, that resolves with paracetamol or ibuprofen, that does not stop you doing things you would otherwise be doing, and that lasts only the first day or two of your period, is within the range of normal. Pain that is severe, that does not respond to simple analgesia, that makes you miss school, work, or social events, that starts earlier in the cycle and lasts beyond the period finishes, that involves pain with sex, urination or bowel movements, or that has been getting worse over time, is not normal. It is also not necessarily endometriosis but it is something that deserves a proper investigation.
How Endometriosis Shows Up
The pain presentations, in the words women use.
There is no one single endometriosis presentation. Women can present at different ages, and different stages of their reproductive life and with different symptom combinations. The disease can be mild, moderate, or severe across each one. What follows are the most common ways endometriosis presents, in the language women themselves use to describe them. If one of these sounds like you, that is worth taking seriously.
The most common presentation. Period pain that is severe enough to make you miss school, work, or social plans. Pain that is not relieved by simple analgesia. Pain that requires you to lie down, to use a heat pack, to take time off. Pain that you have come to plan your life around: scheduling things “after my period,” choosing jobs and study based on whether you can take time off when you bleed, organising travel around your cycle.
This is the pain that women are most often told is “normal.” It is not. Severe period pain is a signal worth taking seriously, even if endometriosis turns out not to be the cause.
Many women describe a slow change over years: pain that used to be limited to the first day or two of bleeding now starts the day before, then a few days before, then mid-cycle, then most of the cycle. This pattern, pain becoming progressively less tied to bleeding, is one of the more characteristic patterns of endometriosis, and it is one that should always prompt investigation.
Specifically, deep pain with sex, often called dyspareunia. The pain is felt deep in the pelvis rather than at the entry to the vagina, and it is often described as worse with certain positions or with deeper penetration. The cause is usually involvement of the ligaments behind the uterus or deep infiltrating disease in the pouch behind the uterus. Surface pain at the vaginal opening is more often vulvodynia or vaginismus, which are different conditions, though they can coexist.
Pain with sex is one of the most under-reported endometriosis symptoms, and there are real reasons for that. Some women have never been asked. Others feel too embarrassed to bring it up. And in the few who do raise it, it has not been met with empathy or taken seriously. But pain with sex is clinically important and treatable, and your doctor cannot help with what they do not know about. At SWW, sex comes up in nearly every consult. You will not be catching us off guard, and we will probably beat you to the punch.
The symptoms that get misattributed for years.
Painful bowel movements around the time of bleeding, particularly with deep infiltrating disease on the bowel. Diarrhoea, constipation, or bloating that follows the cycle. The “endo belly” that some women describe: a marked abdominal distension that comes and goes. Urinary urgency or pain on urination that worsens with the period.
Some bowel symptoms around the period are normal. Your uterus releases prostaglandins to help it shed the lining, and these chemicals also reach the bowel. That is why many women have looser stools or urgency in the first day or two of bleeding, even without endometriosis. The patterns worth investigating are severe pain with bowel movements, symptoms that persist beyond the first day or two, or bowel symptoms that show up at other times in the cycle.
These symptoms are misattributed to irritable bowel syndrome or recurrent urinary tract infections for years before endometriosis is considered. The cyclical pattern is the clue: when symptoms reliably worsen around the period and improve between cycles, the cycle is telling you something.
A heavy, immovable fatigue that does not lift with sleep. It is part of the inflammatory picture of endometriosis and it is one of the symptoms most likely to be dismissed by clinicians, including sometimes by women themselves. If your fatigue is severe, persistent, and cannot be explained by anything else going on, it is part of the clinical picture and it needs to be taken seriously.
For a good number of women, the first sign that endometriosis is in the picture is difficulty getting pregnant. In these women, the delay in diagnosis may be that they have had no significant pain. Others have had pain bearable enough to put up with. And then there are unfortunately those who have had severe pain but have been told it is normal. Another common group are women who have been on hormonal contraception, which has been quietly treating the symptoms for years.
In Australia, the average time from first symptoms of endometriosis to diagnosis is around 7 to 8 years, depending on which study you look at. This is not because endometriosis is impossible to diagnose. It is because pelvic pain in women has been under-investigated because the symptoms have historically been normalised by the medical profession, by society, and sadly even by women themselves.
If you have had pain that fits any of the presentations above, and you have not yet had a proper work up, a reasonable starting point is a GP appointment with the specific request: “I would like to be investigated for endometriosis.” A good GP will take that question seriously, take a careful history, examine you, possibly organise a specialised pelvic ultrasound, and refer you to a gynaecologist if the picture warrants it.
Two things have changed recently that are worth knowing about. From July 2025 there are two new Medicare items for longer specialist gynaecological consultations, a minimum of 45 minutes, for women with endometriosis, chronic pelvic pain and PCOS. The rebate is roughly $168.60 for an extended initial consultation and $84.35 for an extended follow-up, against $95.60 and $48.05 for the standard items. It means the appointment where someone actually takes a full history is now funded to happen. Separately, there are now 33 federally funded Endometriosis and Pelvic Pain Clinics open around the country, including in regional centres, and you do not need a specialist referral to be seen at most of them.
If you have raised this question before and been dismissed, we are sorry, that’s not okay. Don’t let it stop you asking again. Australian guidelines have changed substantially in the last few years. What was reasonable practice ten years ago is not reasonable practice now. If your regular GP is not the right person to revisit this with, or if you find yourself dismissed again, we are happy to help.
Getting a Diagnosis (And Why It Has Become Easier)
What a careful workup actually looks like.
For most of the last century, a formal endometriosis diagnosis required surgery: a surgeon needed to see the lesions during laparoscopy, and in many cases a sample needed to be sent to a lab to confirm it under the microscope, called histological proof. Thankfully this is no longer the position of current Australian or international guidelines, and the shift is one of the more important things every woman with possible endometriosis should know.
In this Part, we walk through what a careful workup actually looks like in 2026, what investigations add what, where laparoscopy still has a role, and what the formal staging system does and does not tell you.
The first and most important investigation is the history. The timing of your pain in relation to your cycle, how the pain has changed over time, what makes it better and worse, whether there is pain with sex, whether bowel and bladder symptoms track with bleeding, whether there is a family history of endometriosis, and what you have already tried. This sounds basic, and it is, but it is also where the diagnosis is most often made or missed. Endometriosis has a recognisable clinical pattern when the right questions are asked.
Then next an examination. A pelvic examination can sometimes detect signs that point toward endometriosis: tenderness in particular spots, nodules along the ligaments behind the uterus, a uterus that is fixed in position rather than mobile. A normal pelvic examination does not rule endometriosis out, and many women with significant disease have a normal examination, but particular findings can strongly point toward it.
Ruling out the look-alikes.
Several conditions cause similar symptoms and need to be considered alongside endometriosis. This is not dismissal. It is part of getting the diagnosis right, because some of these conditions need different treatment, and several of them can coexist with endometriosis, in which case proper treatment needs to address all of them. The common look-alikes:
| Condition | What it is, and why it matters here |
|---|---|
| Adenomyosis | Endometrial-like tissue growing into the muscular wall of the uterus itself. Causes heavy, painful periods and often a tender, enlarged uterus. Detectable on imaging. Very commonly coexists with endometriosis. |
| Fibroids | Benign muscular growths in or on the uterus. Can cause heavy bleeding, pressure symptoms, and sometimes pain. Visible on ultrasound. |
| Ovarian cysts | Cysts on the ovary can cause cyclical pain and are visible on ultrasound. An endometrioma is a particular kind of cyst caused by endometriosis itself, but other ovarian cysts have other causes. |
| Irritable bowel syndrome | Cyclical bowel symptoms, bloating, and abdominal pain that closely mimic the bowel symptoms of endometriosis. Frequently coexists with it. |
| Bladder pain syndrome (interstitial cystitis) | Bladder pain and urgency without infection. More common in women with endometriosis than in the general population. |
| Pelvic floor dysfunction | Tight, reactive pelvic floor muscles. Often a consequence of long-standing pelvic pain from any cause, including endometriosis itself. Treatable with pelvic floor physiotherapy. |
| Pelvic inflammatory disease | Infection of the upper genital tract, usually caused by a sexually transmitted infection. Can leave behind ongoing pain even after the infection has been treated. Worth ruling out with appropriate testing. |
| Pudendal neuralgia | Burning or electric pain in the area supplied by the pudendal nerve, often worse with sitting. |
A careful workup considers each of these, with the weight given to each one shaped by the symptom picture. Some are ruled out by history alone, some need imaging, some need specific tests.
The investigations themselves.
The investigations that are now considered first-line for suspected endometriosis are:
A specialised ultrasound performed transvaginally is the first imaging investigation. In experienced hands, it can detect endometriomas, deep infiltrating endometriosis in the pouch behind the uterus and on the bowel, and adenomyosis. It does not reliably detect superficial peritoneal endometriosis, which is the most common form. This is important: a normal ultrasound does not rule endometriosis out. It rules out the more advanced forms that are visible on imaging.
The quality of the ultrasound matters. A standard pelvic ultrasound performed by a general sonographer is not the same as a specialist endometriosis ultrasound performed by a sonographer trained in the field. If you have significant symptoms, the more specialised scan (sometimes called a “deep endometriosis ultrasound” or “endometriosis-focused pelvic ultrasound”) is the one worth requesting.
Used selectively, usually when deep infiltrating disease is suspected, particularly involvement of the bowel, bladder, or ureters. MRI can map the anatomy in detail and is sometimes used to plan surgery in advanced cases. It is not a first-line investigation for most women, but it is an important option for women who cannot or do not want to have a transvaginal ultrasound, including women who have never been sexually active.
There is no blood test that can diagnose endometriosis. The much-discussed CA-125 is sometimes elevated in endometriosis, but CA-125 is not a screening test for endometriosis and should not be used as one. CA-125 is non-specific, and is also elevated in many other conditions including ovarian cancer, pelvic inflammatory disease, and pregnancy, and a normal CA-125 does not rule endometriosis out.
Researchers continue to look for a reliable blood-based diagnostic test for endometriosis. As of 2026, no such test has been validated for routine clinical use. If you are offered a “blood test for endometriosis” outside a clinical research setting, it is worth asking what is being measured and what the evidence is for it.
What this means for laparoscopy.
The current Australian guidance is the Australian Living Evidence Guideline: Endometriosis, published by RANZCOG. The word living matters: rather than being reissued every few years, it is updated continuously as new evidence lands, which is part of why the advice a woman was given a decade ago can be so different from the advice she would get today. Together with the leading international guideline (ESHRE, 2022 update), it supports clinical diagnosis, with or without imaging, as the standard. Treatment can be started on that basis without surgery.
The reasoning is straightforward: laparoscopy is surgery, with all the usual risks (anaesthetic, bleeding, infection, damage to nearby organs, scar tissue) plus recovery time and theatre access. If a woman is going to be treated medically anyway, surgery purely to confirm a diagnosis adds risk without changing her management. Our position at SWW is to follow the current guidelines and recommend against laparoscopy purely for diagnostic purposes.
There is one exception worth naming. Some women, after years of being dismissed, want surgical confirmation of their disease for their own sense of validation and certainty. This is a reason to consider laparoscopy, and we take it seriously. If you choose this path, two things matter: the risks of surgery are the same whether the operation is for treatment or for confirmation, and need to be discussed honestly; and the surgery should be done by a gynaecologist with specific endometriosis expertise, so that if disease is found, it can be treated in the same operation.
Staging: what it tells you, and what it does not.
When endometriosis is found at surgery, or on specialist imaging, it is often described by stage. Stage I (minimal) is a small amount of superficial disease. Stage II (mild) is a bit more superficial disease, possibly with small endometriomas. Stage III (moderate) is more extensive disease, including endometriomas and adhesions. Stage IV (severe) is extensive deep infiltrating disease and significant adhesions. The stage is calculated by adding up scores for the size, location, and depth of lesions, plus the extent of adhesions.
Here is the part many women are never told: the stage does not correlate well with the pain. A woman with Stage I disease can have severe, disabling pain. A woman with Stage IV disease can have minimal pain. This is one of the clearest signs that endometriosis is not just an anatomical disease. The visible lesions are part of the picture, but the pain experience depends on the inflammatory environment, the nerve sensitisation, the pelvic floor involvement, and the wider context of her physical and mental health. None of these are captured by the staging system.
The staging system is useful for surgical planning, for research, and for communication between clinicians. It is not a measure of how much pain you should be in, and it is not a predictor of how you should respond to treatment.
Stage does not predict pain. Stage I endometriosis can cause severe pain. Stage IV can be silent. Medicine measures what it can see. Pain is not always one of those things.
Treatment: What Works, Medically, Surgically, and Beyond
The foundations come first.
Endometriosis does not have one cause and it does not have one fix. The disease works structurally, hormonally, and through inflammation, and the treatments work the same way, on more than one front at a time. Medical treatment, surgical treatment, pelvic floor physiotherapy, pain neuroscience, and the lifestyle foundations all sit alongside each other as parts of the picture. Most women only think about surgery as the fix for endo, but in reality the heavy lifting is done by more of the others.
Two things to hold in mind before we go in. First, endometriosis is a chronic condition. The aim of treatment, for most women, is to manage symptoms and protect quality of life and fertility over years and decades, not to “cure” the disease in a single intervention. Second, what works for one woman does not necessarily work for another. The biology varies, the symptom patterns vary, and the priorities (fertility, pain control, freedom from bleeding) vary. A good treatment plan is matched to your specific symptoms, stage of life and personal preference.
To be very clear: lifestyle is not a cure for endometriosis. The disease is structural, hormonal, and inflammatory, and it almost always needs medical, and sometimes surgical, treatment to manage properly.
That said, the lifestyle foundations are not optional extras either. Nutrition, movement, sleep, alcohol intake, and stress are the platform on which everything else sits. They have real, well-evidenced effects on inflammation, pain perception, hormone levels, energy, and the body’s capacity to manage a chronic condition over years and decades. A woman with severe endometriosis is not going to manage her disease through diet alone. But a woman with endometriosis who is sleeping five hours a night, eating poorly, drinking heavily, and not moving her body is going to have a harder time, regardless of what other treatment she is on.
Medical management, the first line for most women.
Medical management aims to reduce the activity of the disease by changing the hormonal environment. The principle is straightforward: endometriosis lesions are fuelled by oestrogen and counteracted by progesterone. So most treatments either reduce oestrogen by suppressing ovulation, increase progesterone continuously so there is no cyclical drop, or do both. Less hormonal swing, less lesion activity, less inflammation, less pain.
A short note before the table. All hormonal treatments come with their own profile of side effects, risks, contraindications, and situations where they suit one woman more than another. We cover that detail in our Contraception Deep Dive. Here we focus on what each option does for endometriosis, and we will leave which option is best for you, up to a discussion between you and your doctor.
| Option | What it does for endo |
|---|---|
| NSAIDsibuprofen, naproxen, mefenamic acid | Anti-inflammatory pain relief is the foundation of endometriosis pain management, which should be used by every woman who can. NSAIDs reduce the prostaglandins that drive period pain and contribute to the local inflammation around endometriosis lesions. What they are: over-the-counter or prescription anti-inflammatory tablets. Most useful when started a day or two before your period, rather than after pain has already escalated.Worth knowing NSAIDs do not treat the disease itself. They take the edge off the pain while other treatments work on the underlying inflammation and hormonal environment. |
| Combined hormonal contraceptionthe combined pill, the vaginal ring | Often the first-line medical treatment for endometriosis. The combined pill suppresses ovulation, which removes the cyclical surge of oestrogen that fuels the lesions. It also provides continuous progesterone, which counteracts the effect of oestrogen on the tissue. Less hormonal swing means less lesion activity and less pain. What it is: a daily pill, or a monthly vaginal ring, containing both oestrogen and progesterone.Worth knowing For endometriosis, the combined pill is usually taken continuously, skipping the placebo week, so that there is no monthly bleed and no monthly pain. Continuous use is safe and well-evidenced. |
| Oral progestinsdienogest (Visanne), norethisterone (Primolut N), drospirenone (Slinda) | Oral progestins reduce lesion activity by providing continuous progesterone exposure, which counteracts the effect of oestrogen on endometriosis tissue. They suppress ovulation depending on the dose and the specific progestin, reduce inflammation, and often reduce or stop bleeding entirely. What they are: daily progestin-only tablets. All three are reasonable options for endometriosis, each with their own pros and cons.Worth knowing Dienogest is the only oral progestin specifically licensed for endometriosis in Australia. The others are used off-label for the disease, which is common practice and well-supported by clinical experience. Which one suits you is a conversation with your doctor. |
| Injectable and implantable progestinsDepo-Provera, Implanon | These options work the same way as oral progestins, providing continuous progesterone exposure, suppressing ovulation and reducing lesion activity, but delivered in a different way. For women who don’t want to take a daily tablet, or who find a daily routine hard to keep up with, these can be a good fit. What they are: a three-monthly injection (depot medroxyprogesterone) or a small implant placed under the skin of the upper arm (etonogestrel).Worth knowing Depo can cause temporary bone density loss and is generally not used long-term in younger women without proper consultation. |
| The hormonal IUDMirena | Like oral progestins, the Mirena provides continuous progesterone, but it does so locally rather than throughout the body. The effect is concentrated in the uterus, which makes the Mirena particularly effective for the parts of endometriosis pain that come from the uterus itself. What it is: a small T-shaped device that sits inside the uterus and slowly releases a low dose of progesterone over five to eight years. Inserted in a clinic appointment, no daily dosing, no monthly bleed for most women.Worth knowing The Mirena is particularly effective for adenomyosis, the related condition that very often coexists with endometriosis. Because its effect is mostly local to the uterus, it is less effective for pain coming from lesions outside the uterus, on the ovaries, peritoneum or bowel. Women whose endometriosis sits mostly outside the uterus often need an additional systemic treatment alongside the Mirena. |
| GnRH agonistsgoserelin (Zoladex), nafarelin (Synarel) | A second-line option for women whose pain has not been controlled by hormonal contraception or progestins. GnRH agonists work by switching off the brain’s signals to the ovaries, which stops oestrogen production almost completely. With no oestrogen to fuel them, the lesions become inactive. Highly effective for endometriosis pain. What they are: monthly implants (Zoladex) or a nasal spray (Synarel). Almost always given alongside “add-back” therapy, which is a low dose of hormone replacement to soften the menopause-like side effects and protect bone density.Worth knowing Usually reserved for women who have not responded to first-line treatments, or as a bridge before surgery. |
| GnRH antagonistsrelugolix with oestradiol and norethisterone (Ryeqo) | A newer cousin of the GnRH agonists, working through the same mechanism, reducing oestrogen to starve the lesions, but with two practical advantages: a daily tablet rather than an implant or nasal spray, and the add-back hormones built into the same tablet so it is a single medication rather than two.Worth knowing Ryeqo has been PBS-listed since May 2025, but as a second-line option: the listing is restricted to women who have already had medical or surgical treatment for endometriosis. Treatment is recommended for up to 24 months, with any extension depending on stable bone density, so a DXA scan is needed before starting and each year on it. It can be started by any doctor experienced in managing endometriosis, GPs included. |
Surgical management.
Surgery is considered when medical management has not given enough pain control, when the disease is contributing to difficulty getting pregnant, when there is significant deep infiltrating disease affecting nearby organs, or when the woman has chosen surgical confirmation as part of her own decision-making, with risks understood. The aim of surgery in endometriosis is to remove the visible endometriosis lesions and to release adhesions where these are contributing to symptoms.
Excision versus ablation. Two techniques exist for treating lesions surgically. Excision means cutting the lesion out, including its deeper roots into the surrounding tissue. Ablation means destroying the surface of the lesion with heat or laser, without cutting it out. For deep infiltrating disease, excision is generally preferred because the deeper part of the lesion is left behind by ablation. For superficial disease, the evidence is less clear-cut, and both techniques are used by experienced surgeons. The key, regardless of technique, is that the surgery be done by a gynaecologist with specific endometriosis expertise. Endometriosis surgery is not the same as general gynaecological surgery, and outcomes vary considerably with surgical experience.
Surgery for endometriosis can be highly effective, but it’s not a perfect cure. Removing the visible lesions does not always remove the pain, particularly when the nerves have already become sensitised or there is pelvic floor dysfunction. Surgery itself can also cause new adhesions and new pain. For fertility, the picture is mixed: surgery can improve the chance of conceiving for some women, and can reduce ovarian reserve in others. The right choice depends on the specifics of your disease, your age, your fertility intentions, and the experience of the surgeon. This is a conversation that benefits from a fertility specialist’s input alongside the gynaecologist.
Hysterectomy is not a cure for endometriosis.
For decades, women with severe endometriosis were sometimes told that hysterectomy would cure the disease. It does not, and this matters before considering the surgery.
Hysterectomy removes the uterus. It is highly effective for treating bleeding-related symptoms and for treating coexisting adenomyosis. But endometriosis lesions, by definition, live outside the uterus. Removing the uterus does not remove them. For some women, pain improves markedly after hysterectomy because the uterine component of the pain was significant. For others, pain persists because the endometriosis itself was not addressed, or because the pain has become driven by nerve sensitisation that surgery cannot reverse.
If you are considering hysterectomy for endometriosis, three things matter. The first is that the endometriosis lesions themselves are addressed in the same operation by an experienced excision surgeon. The second is that you may still need ongoing hormonal treatment after the operation, particularly if there is significant disease outside the uterus. The third is that the decision is yours, and is made with a clear understanding of what the operation can and cannot do for you.
Removal of the ovaries (bilateral oophorectomy) is sometimes considered alongside hysterectomy in severe cases, with the reasoning that removing the source of oestrogen removes the fuel for the disease. The trade-off is that removing the ovaries in a younger woman induces surgical menopause, which has substantial consequences for bone, cardiovascular, and brain health, and requires careful management.
Repeat surgery. In a good number of women endometriosis can recur after surgery. Recurrence rates depend on the completeness of the initial excision, on the medical management used afterwards, and on individual disease biology. The general principle: medical management after surgery reduces the rate of recurrence considerably. Surgery without follow-on medical management is more likely to be followed by recurrence than surgery with it.
Repeat surgery is sometimes needed, but the threshold rises with each operation. Each surgery has a risk of leaving behind adhesions. Those adhesions complicate the next operation, and they can also become a source of pain themselves. And if the pain has become driven by nerve sensitisation, more surgery does not change the mechanism. A woman can have lesions removed repeatedly without her pain improving.
The under-recognised pillar: pelvic floor physiotherapy.
If we were to name the single most under-prescribed treatment for endometriosis pain, it would be specialist pelvic floor physiotherapy. The reasoning has been laid out in Part Two: long-standing pelvic pain can produce tight, reactive pelvic floor muscles, and these muscles then become an independent source of pain. Treating the endometriosis without treating the pelvic floor often leaves residual pain that the woman, and sometimes her doctor, attributes to ongoing disease activity when it is actually muscular.
A pelvic floor physiotherapist who specialises in chronic pelvic pain can assess the muscles, teach relaxation and release techniques, work with internal trigger points, and help retrain the pelvic floor to function normally. Many women describe pelvic floor physiotherapy as one of the most useful things they did in their endometriosis treatment, and most of them had to find it for themselves. We recommend it as part of standard care for any woman with significant endometriosis.
Pain neuroscience and central sensitisation.
For women with long-standing endometriosis pain, particularly where pain has persisted after good medical and surgical treatment, the central sensitisation discussed in Part Two needs to be addressed. The approach is different from treating the lesions themselves. It involves understanding how chronic pain rewires the nervous system, working with a pain psychologist or a clinician trained in pain neuroscience education, and sometimes using medications that act on the nervous system. The goal is to settle a nervous system that has spent years on high alert. With the right approach, the pain signals can become quieter over time. Not always gone, but closer to the volume that lets you live your life.
If a clinician suggests pain neuroscience as part of your treatment, that does not mean they think your pain is in your head. Pain neuroscience is a biological treatment. It works on the changes that chronic pain has made to your nervous system, using a combination of education, specific physical therapy, medication, and psychological techniques. The pain is real. The mechanism it is treating is real. It just lives in your nervous system rather than in the tissues themselves.
Endometriosis, like many aspects of women’s health, has attracted a substantial wellness-industry presence. If a woman has spent years in pain, dismissed and undertreated by medicine, of course she will look elsewhere for help. The wellness industry is more than happy to step in. The issue is, unlike medicine, it does not have to prove any of its promises work.
One of its most visible products is the “endo diet”: eating sold as gluten-free, dairy-free, lectin-free, soy-free or low-FODMAP, and every combination of those, marketed specifically as endometriosis treatment.
So what does the evidence actually say? It is mixed. There is some evidence that an anti-inflammatory pattern of eating, more vegetables and fruit, more whole grains and legumes, more fish, less ultra-processed food, less excess alcohol, is linked with somewhat less severe endometriosis symptoms. That is more or less the Mediterranean diet, which is recommended for everyone to live well, not just for women with endo. There is also some evidence that women with endometriosis who also have IBS benefit from working with a dietitian on a low-FODMAP approach. That helps the bowel symptoms specifically. It is not an endo diet.
What there is not good evidence for is that cutting gluten, dairy, soy, lectins, or any other single food group as an “endo diet” reliably reduces endometriosis pain. The studies that have looked at this are small, mostly poorly designed, and the benefits women see, when they see them, are modest.
Our position: an anti-inflammatory pattern of eating is reasonable and probably helpful at the margins. Significant restriction without a specific reason is unlikely to help and can cause its own problems, extra stress and pressure to eat perfectly and in worst-case scenarios disordered eating patterns and nutritional deficiencies. If you want to try dietary changes for endometriosis, working with an Accredited Practising Dietitian, rather than a wellness influencer, is the way to do it. She will know what the evidence supports and what it does not.
Endometriosis and Fertility
The short version, and the mechanisms.
Fertility is one of the most common concerns following an endometriosis diagnosis, and the online information on it is some of the most frightening, least balanced, and least useful you can find. So let us walk through what is actually known.
Endometriosis affects fertility for some women. It does not affect fertility for many others. Most women with endometriosis who want children do. The impact of endometriosis on fertility depends on the severity of the disease, on the woman’s age, on what else is going on, and on what treatments are used along the way.
Endometriosis can affect fertility through several mechanisms. Adhesions can block or distort the fallopian tubes, making it harder for the egg and sperm to meet, which is most relevant in more advanced disease. Endometriomas can reduce ovarian reserve in two ways: through direct damage to ovarian tissue, and through the surgery to remove them. Larger endometriomas, and endometriomas on both ovaries, have a larger effect.
An inflammatory state in the pelvis can also affect ovulation, fertilisation, and implantation. This is the mechanism that is hardest to measure but that probably explains why even mild endometriosis is sometimes associated with subfertility. And there is some evidence that severe endometriosis is associated with reduced egg quality, though the evidence is mixed and the effect, where present, is modest.
The numbers, in context.
Around 30 to 50% of women with endometriosis experience some degree of subfertility. This is higher than the general population, where around 15% of couples experience subfertility, but it also means that around half to two-thirds of women with endometriosis do not have significant fertility problems. Severity matters: women with severe disease are more likely to have fertility implications than women with mild disease, though the relationship is not always that simple.
When to raise it, and what shapes the timing.
There is a temptation to look for a rule here: try for this many months, then get help. The Australian Living Evidence Guideline does not set one. What it says is that a woman with endometriosis should be referred to a fertility specialist when fertility is a priority for her, and that ongoing concern about how long conception is taking is itself a reason to be seen. That is a deliberately softer trigger than the standard advice given to couples without endometriosis, and it is softer for a reason: it puts the decision to seek advice in your hands rather than behind a waiting period.
What still shapes the urgency is your age, because ovarian reserve declines with time regardless of endometriosis, and the pattern of your disease. Deep disease, an endometrioma, suspected tubal involvement, extensive adhesions, reduced ovarian reserve, or previous ovarian surgery all bring the conversation forward. Deep disease is best managed through an experienced endometriosis service.
The question of surgery before fertility treatment is a nuanced area. For some women, surgical excision of endometriosis lesions before attempting natural conception, or before IVF, improves outcomes, and the guideline notes that removing superficial peritoneal disease may improve the chance of a viable pregnancy. For others, the surgery itself can reduce ovarian reserve, particularly when it involves removing endometriomas, and the trade-off is not always worth the risk. The decision is individual and depends on the disease pattern, the woman’s age, ovarian reserve markers, and her priorities. A fertility specialist with endometriosis experience is best placed to walk through the specifics.
The role of IVF.
IVF can be a good option for women in whom endometriosis is contributing to difficulty conceiving. It works around the parts of the body that endo affects most.
The eggs are taken straight from the ovary, which skips past any blockages or scarring that endo has caused in the fallopian tubes. Fertilisation happens in a lab, away from the inflammation in the pelvis, where the strongest embryos can be selected for transfer.
The one thing IVF cannot work around is the uterus itself. Even when the lining is healthy looking, endometriosis seems to make it less ready to welcome an embryo. This is why IVF success rates in women with endometriosis are good, but slightly lower than in women without.
None of this is a guarantee. What IVF is, is the best tool we have for working around the parts of the body that endo affects most.
An endometriosis diagnosis is not a verdict on your fertility. It is information you can plan around.
A note for women not currently trying. If you have endometriosis and anticipate wanting children in future, this is worth raising early with a doctor who has endometriosis expertise.
Endometriosis can affect fertility, mostly through its effect on ovarian reserve, meaning how many eggs you have left, and on egg quality. Both can decline over time, sometimes faster in women with endo than in women without. The good news is that you can do something about it before it becomes a problem. Early fertility preservation, in the form of egg or embryo freezing, lets you set aside eggs from when you are younger and your reserve is at its strongest. If you go on to conceive naturally, the frozen eggs are insurance you never needed. If you end up needing IVF later, having eggs frozen from a younger you gives the cycle a much better chance than starting fresh later.
Your ovarian reserve can be checked with a blood test (AMH) and an ultrasound that counts the resting follicles in your ovaries, called an antral follicle count. Both are worth understanding properly before you read too much into a number. AMH estimates how your ovaries would respond to fertility medication. It does not predict whether you will conceive naturally, and a low result does not mean you are infertile. What these tests give you is information to plan around, not a verdict.
The Long View: Living With Endometriosis
The pattern across reproductive life.
Endometriosis is a chronic condition. For most women diagnosed in their teens, twenties, or thirties, the disease is part of life for up to four decades. The way it behaves changes across that time, and knowing what to expect at each stage makes the long-term picture easier to manage.
For most women, endometriosis is most active and most symptomatic during the reproductive years, when cyclical hormonal change is fuelling the lesions month after month. Within that period, the pattern is not always linear. Many women have periods of flares interspersed between more settled times, sometimes related to identifiable factors (a particularly stressful period, a change in lifestyle, other health conditions), and sometimes not.
Pregnancy and lactation.
Many women find that endometriosis symptoms quieten during pregnancy and during the months of breastfeeding when periods have not returned. The reasoning is straightforward: in pregnancy hormone levels are stable, and for most suppress endometriosis lesions. This is not universal, and some women have ongoing pain during pregnancy, particularly with deep infiltrating disease. For those whose symptoms do quieten, the improvement does not last forever. Symptoms often return when cycles resume. A note for women reading this postpartum: as your cycles return, so does the disease. Active management between pregnancies, and after your family is complete, matters.
Perimenopause and menopause.
Around the perimenopausal transition, endometriosis can become either more or less symptomatic as you move through the transition. By menopause, when oestrogen levels are low, most endometriosis is quiet. Some lesions resolve entirely; others remain but become inactive. This is one of the few areas where the eventual end of the reproductive years brings real relief from a long-standing problem.
The nuanced piece is what happens with menopausal hormone therapy. For women with a history of endometriosis, MHT, sometimes still called HRT, requires a more thoughtful conversation than for women without. The principle is that the oestrogen in MHT can reactivate dormant endometriosis lesions, even decades after they have last been symptomatic. There is more on the whole picture in our Menopause Deep Dive.
For women with a uterus, this is straightforward: combined therapy, oestrogen with progesterone, is the standard, and the progesterone counteracts the oestrogen on both the uterine lining and the endo lesions. For women who have had a hysterectomy, the conversation is less obvious. Normally a woman without a uterus is offered oestrogen-only MHT. But for women with a history of endometriosis, lesions outside the uterus can still be reactivated by oestrogen alone, and in rare cases unopposed oestrogen exposure over years can drive these lesions toward cancer. For these reasons, combined MHT is often recommended for women with a history of endometriosis even after hysterectomy. This is a conversation worth having with a doctor who has experience in both conditions.
The mental health load.
Living with chronic pain affects mental health. Living with chronic pain that has been dismissed for years affects it more. The relationship between endometriosis and depression and anxiety is well-established, and it is part of the disease picture for many women. If you have endometriosis and you are also struggling with low mood, anxiety, or burnout, this is not a separate problem to be hidden. It is part of the disease, and addressing it is part of good care. A good endometriosis management plan attends to both the pelvis and the mind.
Endometriosis Is Real, And It Is Treatable. You Do Not Need Surgery To Be Diagnosed.
You have made it through a long guide on a long disease, and you do not need to remember any of it perfectly. The reframe worth keeping is this: endometriosis is a real, treatable condition, not a tax on being a woman, and the evidence for how to diagnose and manage it has moved a long way in the last five years.
Now that you understand the why, the next step is a small and specific one. Book the appointment, and ask to be investigated for endometriosis. The average woman in Australia waits 7 to 8 years for that sentence to be taken seriously. You have just spent 45 minutes making sure you do not have to.