Mind & body, in brief

Endometriosis is tissue like the lining of the womb growing outside the womb - most often on the ovaries, the ligaments behind the womb, the bowel and the bladder. [1][3]

It affects about one woman in ten of reproductive age, roughly 190 million people, and there is no cure. [3][11]

The lesions are driven by oestrogen, the main female sex hormone, and as they grow they build their own blood vessels and their own nerve endings. [1]

The commonest kind lies flat on the lining of the belly, and neither an ultrasound nor an MRI scan reliably shows it. [1][6]

So for decades the only accepted proof was a laparoscopy: a camera pushed through a small cut in the belly, under general anaesthetic. [1][5]

In England the average wait from first symptoms to that answer is nine years and four months, and about eleven years for women from ethnic minority communities. [5][6]

In March 2026 the American College of Obstetricians and Gynecologists told doctors they may diagnose endometriosis from symptoms and an examination, and start treatment without operating. [2]

The same guidance makes an ultrasound the first scan, keeps MRI for working out detail, and advises against using blood markers to diagnose. [2]

It covers teenagers as well as adults, because the pain usually starts years before anyone reaches a specialist. [2]

A normal scan still does not rule the disease out, and a woman with the symptoms should be treated anyway. [1]

How much it hurts does not track how much disease there is - a few flat spots can hurt more than a large cyst. [1]

Symptoms sit in several bodies of medicine at once: painful periods, pain during sex, pain passing stool or urine, exhaustion, and trouble getting pregnant. [1][2]

Why it matters. Watch whether the shorter route is actually taken: the test of the new guidance is whether family doctors start treatment on the symptoms, or keep sending women for the operation anyway. [2][9]

The National Institute for Health and Care Excellence, which decides what England's health service uses, has recommended two non-invasive endometriosis tests for family doctors while more evidence on their accuracy is gathered. Until now the only way to confirm the disease in the UK was an operation. Endometriosis affects about one in ten women of reproductive age there, roughly 1.5 million people, and the average wait for an answer is over nine years. Some experts called the tests game changing. [5]

Why it matters. It moves the first real test out of a hospital operating list and into a ten-minute appointment, which is where nearly every woman with these symptoms starts. [5]

Researchers at the University of Oxford in England injected 19 women with a tracer called maraciclatide, which sticks to tissue busy growing new blood vessels, then scanned them. The commonest form of endometriosis sits flat on the lining of the belly and usually does not appear on an ordinary scan, which is why surgery was needed to find it. In this pilot it showed up. Much larger trials are required before any hospital can use it. [6][7]

Why it matters. If it holds, finding the disease stops depending on an operating theatre and starts depending on a scanner slot, which hospitals have far more of. [6]

A trial run by the gynaecologist Donna Ghosh at a hospital in Worcestershire, England, is testing whether endometriosis can be spotted from the electrical activity of the small intestine. Small electrodes are stuck on the abdomen, and the pattern of that activity is reported to differ in women with the disease. It began in November and is still recruiting women with no history of pelvic pain as comparisons. One patient interviewed said the prospect of surgery at 14 frightened her into waiting four more years. [42]

Why it matters. It is one of several attempts to replace the operation with something a nervous teenager would agree to on the day. [42]

A test measuring three microRNAs, three proteins and one hormone in a blood sample was built on 218 women and checked on a separate 80. MicroRNAs are short pieces of genetic material that circulate in blood and change with disease. In the check group the test picked out cases with a sensitivity of 0.80 and a specificity of 0.975. It also identified 61.5% of surgically confirmed cases that ultrasound or MRI had missed. [38]

Why it matters. Those missed cases are the ones the scan-first route sends home, so a test that catches them changes who reaches treatment at all. [38]

Researchers sequenced microRNAs in serum, saliva and vaginal mucus from 20 women, ten with endometriosis and ten without. The three fluids gave different profiles: thirteen microRNAs differed in serum, six in vaginal mucus and only three in saliva, with saliva carrying the fewest overall. Serum results were then matched against 59 proteins raised in the same samples. Twenty women is a very small study. [33] A separate review notes a saliva signature of 109 microRNAs that has been developed into a product. [39]

Why it matters. It matters which fluid the test uses, because a saliva kit posted to a house and a blood draw at a clinic reach different people. [33]

A separate study sequenced blood microRNAs from 20 women with endometriosis and 20 without, and trained a machine-learning model that reached 90% or better accuracy. When the same markers were re-measured with qPCR, a cheaper laboratory method that a hospital could actually run, some of the findings held and some did not. The authors describe the gap between discovery and routine testing as the hard part. [34]

Why it matters. A marker can look strong on a research sequencer and weaker on the cheap laboratory machine a hospital would actually run, and that gap is where most promising tests stop. [34]

Most microRNA work on endometriosis has been done in European and East Asian groups, and the patterns have not always repeated across populations. An Indian team picked nine circulating microRNAs that had been reported consistently, then measured them in 12 women with advanced endometriosis and 11 without, all confirmed by surgery. The numbers are small and the authors say so. [35]

Why it matters. A test that only works in the population it was built in would move the diagnosis queue in some countries and not others. [35]

A team collected menstrual blood from 42 women, 19 with endometriosis and 23 without, isolated the stem cells it carries and read the chemical marks that switch genes on and off across the whole genome. The marked regions clustered in genes for inflammation and tissue remodelling, and told the two groups apart. Period blood is normally thrown away; one US company has been asking women to post used tampons to a laboratory in Oakland, California. [36][11]

Why it matters. It is the one sample a woman with these symptoms already produces every month, and nobody has to book anything to get it. [11]

Researchers measured 96 inflammatory markers in the blood of 86 women having surgery for suspected endometriosis, then sorted them by computer into groups. The women sorted into five distinct clusters rather than one group. The presence of a fibroid, a common non-cancerous growth in the womb muscle, shifted the marker profile and could hide the endometriosis signal underneath it. [37]

Why it matters. Any blood test for endometriosis has to work in women who also have fibroids, and here the fibroid moved the reading. [37]

The US National Institutes of Health is running a competition, the ACT ENDO Challenge, for teams building diagnostic technology for endometriosis. Entrants submit a prototype; winners of the second phase get $100,000 each, and those who reach the development sprint compete for a further $350,000 to $850,000 apiece. The brief states plainly that diagnosis can be delayed up to ten years, partly because intense period pain gets treated as normal and partly because proof required surgery. [40]

Why it matters. A public prize is what gets offered when nobody has brought a working test to market on their own. [40]

Researchers interviewed 52 people with endometriosis in the United States and describe a pattern they call diagnostic buck-passing. A woman with pelvic pain is sent from one specialist to the next; each rules out the organ they know and refers her sideways. One woman was given a scoliosis diagnosis for her back pain, then sent to a gut specialist who suggested irritable bowel syndrome, and was told she was fine at several emergency visits. She was diagnosed at 30, ten years after the pain started. [8]

Why it matters. Nobody in that chain refused her. The referral that would have found it was simply never the one anybody wrote. [8]

Fifteen British healthcare professionals - family doctors, gynaecologists and nurses - took part in focus groups about why endometriosis takes so long to diagnose. Three themes came out of the transcripts. One they named the power of the witness: the patient alone was not always enough, and the presence of another person, most often a male partner, made it easier for the clinician to cross the threshold to referral. The authors ask colleagues to notice themselves doing it. [9]

Why it matters. The referral is a human decision, and this study found something that moves it which is not in the patient's body at all. [9]

A cross-sectional study of Japanese women split them by how long their diagnosis took. Those in the long-delay group waited 2.7 years from their first symptom before even seeing a gynaecologist, against 1.3 years for the short-delay group. Stage IV disease, the most extensive, was commoner among the long-delay group and stage I commoner among the short. Distress scores were higher too, 4.16 against 3.48 on a ten-point scale. Women who used over-the-counter painkillers were more than twice as likely to be in the long-delay group. [10]

Why it matters. Painkillers that work well enough to get through the day also postpone the appointment, and the disease keeps going while they do. [10]

A meta-analysis pooled 127 studies covering nearly 199 million women. Endometriosis turned up in 5% of the general population, 38% of women being treated for infertility, and between 18% and 42% of women attending with gynaecological symptoms. Adenomyosis, the related condition inside the womb muscle, ran at 1% in the general population and 31% among women with infertility. The authors note the figures move with which diagnostic method the study used. [4]

Why it matters. These are not five different diseases. They are five different groups of people, sorted by how closely anyone was already looking. [4]

A team at the University of Oxford used UK Biobank records from more than 8,000 women with endometriosis and close to 65,000 with immune-related conditions, and tested the link against 31 diseases including multiple sclerosis, coeliac disease and psoriasis. Women with endometriosis had a 14% higher risk of one immune condition, and a 21% higher risk of having at least two. A meta-analysis this year also found a 23% higher risk of heart and blood-vessel disease. [12]

Why it matters. It is evidence for treating endometriosis as a whole-body immune illness rather than a local problem in the pelvis, which changes who studies it. [12][31]

A review sifted 1,209 papers published between 1927 and 2025 and kept 198. The consistent findings: macrophages, the immune system's cleaners, shift into a form that tidies rather than attacks; natural killer cells, which normally destroy stray cells, kill less well; and regulatory T cells, which hold the immune system back, increase. Backwards menstruation happens in most women, so the difference is thought to lie in what does not clear it. [13]

Why it matters. The tissue arriving is ordinary. What is unusual is that it is allowed to settle and stay. [13][30]

One group read 108,497 single cells from the wombs, lesions and surrounding tissue of 14 patients and sorted the macrophages into five states. The kind that dominated ovarian lesions sat around blood vessels and switched on programmes for tolerance and for growing new vessels, while turning down the machinery it uses to show a threat to the rest of the immune system. In short, the cleaner was building instead of clearing. [15]

Why it matters. It gives a target: a drug that changed which state those cells sit in would act on the lesion itself, not on hormones. [15]

Complement is a set of blood proteins that mark damaged or foreign tissue for destruction. In endometriosis, cells inside the lesions themselves make and release complement components, and the products of that pathway drive inflammation, encourage new blood vessels and help the tissue invade further. The same system that should be removing the tissue ends up feeding it. [16]

Why it matters. It is one reason drugs that simply damp inflammation have disappointed: some of the inflammation is doing the building. [16][13]

A review of T cells in endometriosis notes that around 95% of women with the disease report at least one other condition - inflammatory bowel disease, irritable bowel syndrome, asthma or rheumatoid arthritis are the common ones. Several of those are themselves driven by T cell trouble, so the same immune fault may be running in more than one diagnosis at a time. [14] A separate review sets out the molecular routes shared with those inflammatory and autoimmune conditions. [32]

Why it matters. It explains part of the diagnostic maze: one woman carrying four labels is treated in four clinics at once, which is the pattern the buck-passing interviews describe. [14][8]

New sensory nerve fibres grow into endometriosis lesions alongside new blood vessels, and immune cells and nerve endings then signal back and forth to each other. Reviews now describe this nerve-and-immune traffic as a driver of the disease itself, not just of the pain: the signalling changes how the lesion's own cells behave. Nerve growth also runs on the hormone signals that make the lesion grow. [17][18]

Why it matters. A lesion with its own nerve supply is why a small patch can hurt far more than a large one. [17][1]

Mast cells are immune cells packed with histamine, the chemical behind an allergic reaction. Oestrogen activates them directly inside endometriosis lesions. When they fire they release histamine and a growth factor called FGF2, which make nearby nerve endings more sensitive and increase the traffic arriving at the spinal cord. That in turn recruits more of them, so the pain feeds itself. [19]

Why it matters. It is a concrete target for pain that hormone treatment does not settle, and there are already drugs that act on mast cells. [19]

Researchers compared rhesus macaques that develop endometriosis naturally with mice given repeated lesions. In both, glial cells - the nervous system's support cells, which also amplify pain - stayed switched on across several brain regions and the spinal cord long after the trigger. Two drugs, the hormone treatment dienogest and the immune drug fingolimod, both reduced the animals' pain sensitivity and the inflammation in the nervous system. [20]

Why it matters. It is direct evidence that the pain outlives the lesions, which is why removing them does not always end it. [20][44]

Sixty-six women with deep endometriosis rated their pain, and the researchers found nerve fibre growth and pain of the kind that comes from damaged nerves rather than from inflammation alone. In a mouse version, cells in the spinal cord called microglia switched into an inflammatory state through a specific signalling pair, and blocking it reduced the pain. Lesions starved of oxygen appeared to be what set the process off. [21]

Why it matters. Pain that has moved into the spinal cord will not answer to a gynaecologist's tools, which is a different clinic and a different waiting list. [21]

Forty-three people with surgically confirmed endometriosis, aged 12 to 44, had structural brain scans alongside psychological tests, compared with 26 people never diagnosed and with no pelvic pain. Two regions - the fusiform gyrus and the lateral occipital cortex - were smaller in the endometriosis group, and thinning in a frontal region tracked with age only in that group. It is a snapshot, not a film, and cannot say which came first. [22]

Why it matters. Researchers are now looking in the brain for what years of untreated pain leave behind. [22]

Two hundred women treated for endometriosis pain between 2020 and 2024 were assessed with standard questionnaires and had blood inflammation markers measured. Clinically significant depression appeared in 42.5% and anxiety symptoms in 51.0%. Levels of interleukin-6, interleukin-1 beta, tumour necrosis factor alpha and C-reactive protein - all signals the body raises during inflammation - were higher in those with the worst scores. [23]

Why it matters. It gives an alternative to the oldest explanation offered to these women, which was that the distress came first and produced the pain. [23]

The fluid in the belly around the lesions carries far more oestrogen and progesterone than blood does. A review argues that the reason the contraceptive pill relieves endometriosis pain is that stopping ovulation lowers oestrogen in that fluid, and that a direct progesterone effect is unlikely because progesterone there is already high. It also notes that pill doses are much higher than needed to stop ovulation - in most women half would do, and a pilot in eight adolescents tested the idea. [24]

Why it matters. If the dose can come down without losing the effect, the side effects that make young women stop taking it come down too. [24]

For years the field has held that one particular oestrogen receiver, ER beta, is unusually abundant in endometriosis lesions and would make the first drug aimed at the lesion rather than the symptoms. A group pooled single-cell data from eight published studies and looked at which cells actually carry it. Their re-analysis does not support the idea as stated. [25]

Why it matters. A target that gets funded on the strength of a hypothesis is worth re-checking before the trials are built on it. [25]

Endometriosis is named for the tissue outside the womb, but the lining inside it is also altered: more inflammatory immune profiles, changed blood-vessel growth and low oxygen, all of which affect whether an embryo can settle. Separately, work across several kinds of measurement finds local oestrogen dominance together with progesterone resistance, meaning the tissue stops responding properly to the hormone that normally calms it. [26][51]

Why it matters. It explains why removing the lesions does not always restore fertility - the surface an embryo has to attach to has changed as well. [26]

Researchers built an atlas of 466,371 cells from womb lining donated by 35 women with endometriosis and 25 without, none of them on hormone treatment. They found raised inflammation, adhesion, cell survival and blood-vessel growth across several cell types. Neural network models trained on the atlas predicted disease with a median area under the curve of 0.83, and one model used just eleven genes. [27]

Why it matters. Eleven genes is few enough to become a laboratory test on a sample of lining, which is taken in a clinic rather than an operating theatre. [27]

Having a first-degree relative with endometriosis raises a woman's risk by three to nine times, and twin studies point the same way. Reviews of the genetics implicate genes for inflammation, immune response, hormone production, new blood vessels and DNA repair, along with stem cells from the bone marrow and the womb lining. A separate review of adolescent cases argues that some of them start developmentally, before birth. [1][28][29]

Why it matters. A disease with a strong family pattern is also one where the pain gets normalised across generations, because the mother had it too. [2][29]

Almost every explanation of endometriosis starts from backwards menstruation. A review argues that this cannot carry all of it: the superficial patches, the deep invading nodules and the ovarian cysts look and behave differently, and forcing one origin onto all three requires too many assumptions. Different origins leave different signatures in the tissue, and those are not part of the standard laboratory report. [30]

Why it matters. If the three kinds are really three diseases, one test and one drug would each be aimed at a mixture, and trials have failed that way before. [30][25]

Nobody has ever run a randomised trial comparing surgery with hormone treatment for deep endometriosis, and a British trial set out to. It screened 377 patients, found 103 eligible and randomised 18, against a target of 320. Of the eight assigned to surgery, one had had the operation by the time the trial closed. Not one participant reached the 18-month point the trial was built to test. Roughly one patient in fourteen has a serious complication from this surgery. [43]

Why it matters. The two treatments a woman is asked to choose between have never been compared head to head, and the attempt to compare them collapsed. [43]

In one retrospective study of 401 patients followed for a median of two years after surgery, pain returned in 34% while lesions were seen again on ultrasound in 16%. A review of recurrence argues that the gap is the interesting part: pain can be driven by changes in the nervous system, by other pain conditions, or by scarring and adhesions from the operation itself. [44]

Why it matters. Counting recurrence by what a scan shows will always find less of it than the women report, and the operation itself is one of the causes. [44][20]

A review pooled seven studies covering 2,101 women who had surgery for endometriosis, splitting those who had one operation from those who had two or more. The odds of becoming pregnant naturally were 2.1 times higher after a single operation than after repeat surgery. Repeat operations are common because symptoms return. [45]

Why it matters. Each operation removes disease and takes some ovary or leaves new scar tissue, so the treatment for returning pain also lowers the chance of getting pregnant later. [45][44]