Learn Body Literacy (2025)

19/11/2025

lesions trigger ongoing inflammation and many immune signaling molecules called cytokines. Researchers have found that patients have abnormal levels of cytokines in the fluid of the pelvis and sometimes in the blood.

Many different immune cells can produce the same cytokine. The immune system is highly redundant, meaning multiple cell types can release the same signaling molecule to ensure that essential responses still occur even if one cell type is absent or impaired.

TLDR; Endometriosis involves a complex mix of heightened inflammation and weakened immune clearance, driven by many interacting cytokines. This imbalance helps lesions survive, grow, and causes symptoms.

Cytokines:

IFN-γ: Normally helps activate immune cells. Levels are inconsistent in studies, but it may be elevated near endometriosis lesions. The abnormal cells may become resistant to its signals that would normally trigger cell death.

IL-1: A strong inflammatory cytokine made by macrophages. It encourages other inflammatory signals, blood vessel growth, and cell proliferation. IL-1 levels are often higher in those with endometriosis and may contribute to pain, inflammation, and infertility.

IL-2: Helps activate T cells and NK (natural killer) cells. Studies conflict, some show reduced IL-2, others show increases, especially in patients with infertility. Its exact role remains unclear.

IL-6: Produced in large amounts by activated macrophages. High IL-6 levels support chronic inflammation, help lesions survive by protecting them from immune attack, and reduce NK cell activity.

IL-8 & TNF-α: Both are increased in endometriosis. They attract immune cells, promote inflammation, and can stimulate the growth and adhesion of endo.

IL-10 & IL-4: These are anti-inflammatory cytokines. They tend to be higher in the pelvic area of those with endo and may weaken the immune system’s ability to remove abnormal tissue.

TGF-β: Also elevated in the pelvis. It can suppress NK cell activity, which may make it easier for lesions to implant and survive.

VEGF: A growth factor that promotes new blood vessel formation. High VEGF levels may help lesions develop their own blood supply.

17/11/2025

T cells are immune cells that help the body recognize and respond to problems like infections or abnormal tissue. Different types have different purposes:
- CD4 T cells coordinate immune responses
- CD8 T cells destroy harmful / abnormal cells
- Th1/Th2/Th17 cells release different signaling molecules
- Regulatory T cells (Tregs) keep the immune system from overreacting

research clearly shows the immune system behaves abnormally. This has been studied using the fluid around the pelvic organs (peritoneal fluid). Some studies found higher levels of signals usually linked to Th2 cells, which normally support healing and scar formation, but the full Th2 pattern doesn’t consistently appear. At the same time, blood samples sometimes show more Th1-type activity, making the overall picture mixed. This is part of the inconsistency around this condition regarding biomarkers.

People with endometriosis often have more CD4 and CD8 T cells in their peritoneal fluid, and the ratio between them (CD4/CD8) can be higher. Some studies report no major changes in blood, while others find fewer CD8 cells in circulation, which also raises the CD4/CD8 ratio. There is also an increase in Th17 cells and their signals (like IL-17) in the pelvic environment, which may worsen the disease by promoting inflammation and new blood vessel growth.

Regulatory T cells normally calm the immune system and help it tolerate the body’s own tissues, but with endo many studies find excess Tregs in the peritoneal fluid. This instead may weaken the body’s ability to clear endo lesions. Interestingly, most research shows no major difference in Tregs in the bloodstream, suggesting their effects are mainly localized.

The takeaway from this is that endometriosis shows a lot of *localized* alterations, in this case to the immune environment, with shifts in several T-cell types that promote inflammation and make it harder for the body to clear the lesion tissues.

More info from this study:
https://doi.org/10.3390/cells11132028

16/11/2025

Something we don't see everyday, a new fertility awareness study, this one is out of Germany. This six month observational study looked at the effectiveness of using salivary progesterone to measure fertility. This is a type of sympto-hormonal method with a digital interpretation (algorithm). The current sympto-hormonal methods utilize LH, estrogen (E3G), or both, but progesterone has long been a neglected hormone in fertility monitoring technology.

The method worked about 96% of the time, and based on the data collected, the researchers are pretty sure the real effectiveness is somewhere between 93% and 98%. This study only adds to the knowledge base that fertility awareness methods that utilize fertility biomarkers are scientifically sound.

This research really makes me think about how many different ways there are to look at fertility. Despite not being keen on an algorithmic interpretations because of their failure to account for human/environmental changes to the cycle, which would probably be the end goal of a product like this one, I am still fascinated with progesterone being easily self monitored.

And I'm encouraged anytime I see ANY research on fertility awareness, because there is very little new work out there. We will continue to see more of this interest rising as technology sectors look for more ways to sell us body-surveillance, so we should always be aware of that angle as well!

15/11/2025

is increasingly understood as an immunologically driven disease. Key innate and adaptive immune cells such as neutrophils, macrophages, NK cells, and T-cell subsets shape the inflammatory microenvironment that supports endo lesion growth. Let's explain!

are elevated in both blood and peritoneal fluid of affected patients, likely due to increased chemotactic factors such as IL-8 and ENA-78. In experimental models, they infiltrate ectopic tissue early and amplify inflammation through IL-17A, VEGF, and CXCL10. Estrogens may influence their activity, though their precise role remains unclear.

are abundant and functionally altered in endometriosis, displaying reduced phagocytic capacity (how they ingest other cells) but heightened production of inflammatory mediators that promote lesion survival, angiogenesis (developing a blood supply) , and proliferation. Their close association with nerve fibers and modulation by estradiol may help explain disease-related pain.

show consistently reduced cytotoxicity (the ability to damage or kill cells) against endometriosis lesions. Abnormal receptor expression, along with suppressive cytokines such as IL-6, TGF-β, and IL-15 in peritoneal fluid, further dampen NK activity. Interactions between stromal cells and macrophages intensify this suppression, contributing to immune escape and possibly higher autoimmunity rates.

responses are complex with end. Peritoneal fluid shows a higher CD4/CD8 ratio and increased T-cell concentrations within lesions. Th17 cells and IL-17 are elevated and correlate with disease stage, promoting angiogenesis and inflammation.

Regulatory T cells ( ) are increased locally in the peritoneal cavity, suggesting microenvironment-specific immunosuppression that protects ectopic tissue. Peripheral levels remain unchanged.

Because endometriosis is characterized by a disrupted immune landscape where altered neutrophil, macrophage, NK cell, and T-cell activity drives chronic inflammation, immune tolerance, and lesion persistence, we should shape our endometriosis care around targeted immunotherapies which address these conditions.

13/11/2025

You're invited! Introducing the first-ever Body Literacy Symposium! 🔬

In January, we'll convene a virtual conference dedicated to advancing menstrual health education. We're coming together as leading experts, practitioners, and advocates to share insights, challenge misconceptions, and promote body literacy for all.

If you’re passionate about menstrual health, fertility awareness, midwifery, or reproductive wellness, I'm so excited to welcome you to this space. Let’s shape a future where evidence-based, informed reproductive health is accessible to everyone. There are some AMAZING projects in this conference and I can't wait to highlight each and every one of them!

To register, click the SYMPOSIUM link in my bio or visit www.learnbodyliteracy.com/symposium to learn more! 🩷

06/11/2025

This is one of those medical myths that remains deeply entrenched. When you interact with physicians and other medical staff, you have no idea if they were informed about the disease through the false lens of retrograde menstruation.

Unfortunately, for decades we were told that endometriosis happens because menstrual blood flows backward into the pelvic cavity. But we know MUCH more now, and the fact of that matter is that while retrograde menstruation happens in most people with me**es, most of them do not develop endometriosis.

If you need to explain to anyone (physicians included) why is NOT simply retrograde menstruation, here's a quick list you can refer to

1. This one I already mentioned briefly: Retrograde Menstruation Is Common, But Endometriosis Is Not In The Total Menstruating Population
2. Endometriosis Occurs in People Without a Uterus or a Menstruation
3. Endometriosis Has Been Found in Fetuses and Neonates
4. Immune Dysfunction Plays a Major Role
5. Retrograde Flow Doesn’t Explain Extrapelvic Endometriosis
6. Lesions Make Their Own Estrogen, Endometrium Does Not

And the list goes on!

When doctors falsely claim that endometriosis is simply retrograde menstruation, they dismiss patients, delay diagnosis, and limit treatment options.

In order to properly address this condition we must research, identify, name, and TREAT the root causes. Too often gynecology leaves those conditions rooted in immune dysfunction underserved because of the limits of the speciality. It’s essential that we understand there are various factors that contribute to the disease pathophysiology and pathogenesis, because this misinformation most often leads to failed concepts of treatment like hysterectomy, drug therapy, and incomplete surgery.

Endometriosis deserves real research.
Patients deserve real care and compassion.
Check out my new course: ENDOMETRIOSIS ESSENTIALS to learn more! 🔬

14/09/2025

The Heterogenous Architecture of Endometriosis 🧬

Endometriosis is increasingly recognized as a heterogeneous disease entity with multifactorial origins. Rather than arising from a single pathway, its pathophysiology reflects the convergence of genetic, epigenetic, hormonal, immunological, metabolic, and environmental factors.

Current evidence highlights several key contributors:
- Hormonal influences: in utero exposures, impaired estrogen metabolism, progesterone resistance
- Immune dysfunction: innate and adaptive immune disruption, altered microbiome composition
- Genetic and epigenetic factors: heritable risk variants and gene regulation changes
- Environmental exposures: endocrine-disrupting chemicals, stress-related HPA axis dysregulation
- Local tissue environment: iron overload, oxidative stress, hypoxia, neuroangiogenesis, and pro-pain signaling cascades

This heterogeneous architecture underscores the variability in clinical presentation, ranging from chronic pelvic pain and infertility to systemic manifestations involving gastrointestinal, urinary, neurological, and even cardiopulmonary systems.

It also exposes why endometriosis is often dismissed. This variability means presentations may not fit the "classic" profile that many clinicians are trained to recognize. As a result, patients experiencing the "non-classic" gastrointestinal, neurological, or systemic symptoms may be misdiagnosed or dismissed, contributing to the well-documented diagnostic delays and gaps in care for endometriosis. Sadly, "classic" endo here is a stand-in for how endometriosis has been misconstrued through initial, incorrect, and sexist research, and these ideas have permeated the medical field, affecting patient care directly.

The complexity of endometriosis necessitates precision medicine approaches, moving beyond generalized symptom management toward individualized diagnostics and therapeutic strategies. In ENDOMETRIOSIS ESSENTIALS, we use quizzes to help you better understand your specific manifestation of endometriosis. Finding which factors are more prominent for you will help you in your approach towards holistic strategies of healing and long term support.

13/09/2025

✨ Why You Should Take Endometriosis Essentials ✨

If you’re living with endometriosis, you may already know how exhausting it is to feel unheard, dismissed, or left without answers from your doctors. That’s why Endometriosis Essentials was created, to empower you with knowledge and tools your healthcare team may not provide. If you're a practitioner that works with people with endometriosis, you'll also benefit from this research deep dive and to explore best protocols.

📚 What the course covers:
- What endometriosis really is (beyond just “period pain”)
- Where it can appear in the body and how symptoms vary
- Common myths vs. facts
- Treatment options explained in detail: surgery, medical management, and holistic support
- Strategies for advocating for yourself in the healthcare system
- Daily lifestyle tools to help manage pain, fatigue, and flare-ups

💡 Why it’s worth it:

- You’ll gain clarity about the medical science known about your condition
- You’ll feel empowered to make informed decisions
- You’ll discover practical strategies you can use right away
- You’ll join the Learn Body Literacy community that validates your experience instead of dismissing it

If you’ve been struggling with endometriosis and feeling let down by your healthcare team, ENDOMETRIOSIS ESSENTIALS gives you the foundation to understand your body, advocate for your needs, and reclaim your quality of life.

12/09/2025

One thing you learn in ENDOMETRIOSIS ESSENTIALS is that is a full-body disease. It characterized by the presence of pain and/or endometriosis lesions, and they don't just grow on the reproductive system. Research shows it can affect multiple organs and systems throughout the body. Even where the lesions don't grow directly, they can cause indirect damage through inflammation and incomplete treatment can cause scarring.

Pelvic Endometriosis may be found:
- On the ovaries
- On the uterus / uterine tubes
- On the bowels
- On the bladder

Extra-Pelvic Endometriosis has been documented in:

- The chest cavity
- The lungs
- The diaphragm
- The liver
- The stomach
- The brain / brain stem
- The pelvic nerves and sciatic nerve

This widespread distribution helps explain why symptoms vary so widely, from pelvic pain and infertility, to digestive, urinary, respiratory, and even neurological issues.

Endometriosis is a SYSTEMIC disease, and it's time we start treating it as such, the medical establishment will just have to catch up 🤷‍♀️. Raising awareness of its full-body impact is critical for better diagnosis, treatment, and support! We have to start broadening the scope and looking at the "why" behind endo, in order to best serve the people struggling with this condition. That means looking holistically, at the whole body.

In ENDOMETRIOSIS ESSENTIALS, the entire course is designed around the fact that endo likely will not be limited to the reproductive system or period pain alone (1 in 2 have extra-reproductive endo growths), and an entire module is dedicated to the extra-pelvic forms of endo, and what we know about them so far (they are quite diverse in how they express!)

If you’re living with endometriosis, your experience is real, valid, and deserves recognition. You deserve universal, compassionate healthcare that is backed by the latest research.

If you want to know more about ENDOMETRIOSIS ESSENTIALS, click the link in the bio!

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