When it comes to fibroids, most women are told the same thing: “They’re benign,” “They’re common,” “We don’t know what causes them,” or worse, “They’re incurable.” But what if the real issue and true nature of how and why they form is being overlooked entirely?
At the cellular level, fibroids are structured, active tissues shaped by biochemical and hormonal imbalances, and one of the biggest overlooked players is the extracellular matrix (ECM). This is the connective tissue framework that holds cells together, much like scaffolding in a building. But in fibroids, that scaffolding becomes excessive, rigid, and dysfunctional.
So why is this not part of the conversation between doctors and the very women affected by fibroids? Are medical professionals even fully aware of the role of the ECM, collagen deposition, and cellular signalling in fibroid development? And if they are, why is this knowledge not being used to help women make sense of their symptoms and find a path to true healing?
Excess Collagen Deposition
Fibroids are dense, fibrous structures packed with collagen, especially type I and type III. Type I collagen is the most abundant in the human body, found in skin, bones, and tendons. Type III collagen is typically found in soft tissues and is associated with wound healing and tissue repair.
In a healthy uterus, collagen is present in moderate amounts to provide structure and elasticity. But in fibroids, the levels are significantly elevated, making them stiff and rubbery to the touch. This dense collagen matrix not only gives fibroids their bulk but also makes them resistant to breakdown and healing.
This excess collagen is a biological response gone awry. But most women have never been told this. And once you understand what’s behind this collagen build-up, you can start to ask a different question: What is driving this overproduction, and how can it be reversed?
Dysregulated ECM Turnover
The extracellular matrix (ECM) is meant to be dynamic, it’s constantly being broken down and rebuilt in healthy tissues. This is known as ECM turnover. Enzymes called matrix metalloproteinases (MMPs) help degrade old ECM components, while fibroblasts and other cells build new ones.
In fibroids, this system is broken. ECM production is ramped up, while degradation is slowed down. One 2010 study in Human Reproduction Update explained that fibroid tissues show a consistent increase in ECM proteins and a decrease in the enzymes responsible for breaking them down.
The result? Tissue accumulation and expansion… a breeding ground for growth. The body is laying down too much structure and not clearing enough away. It’s like a construction site where the builders keep adding bricks but no one ever cleans up the debris.
Again, the question arises: Why is this happening? And more importantly, what can you do to restore balance?
Growth Factor Storage & Release
The ECM also functions as a reservoir for signalling molecules like growth factors. One of the most influential in fibroid development is Transforming Growth Factor-beta (TGF-β). This growth factor does several things:
Stimulates the production of collagen and other ECM proteins
Suppresses ECM-degrading enzymes
Encourages fibroid cell proliferation
Studies, including those in the Journal of Clinical Endocrinology & Metabolism, have consistently shown that TGF-β is overexpressed in fibroid tissue. In short, the ECM stores this growth factor, then releases it in bursts, stimulating more collagen production and more fibroid growth. Its a vicious cycle.
Most women have never heard of TGF-β, let alone its role in fibroid development. But if you knew your fibroids were being fuelled by this biochemical loop, wouldn’t you want to know how to disrupt it?
Stiffness & Cellular Signalling
The rigidity of the ECM in fibroids actively influences cell behaviour. In a soft, flexible environment, cells behave normally. But in a stiff ECM, cells receive signals that promote:
Abnormal cell proliferation (too many cells forming too fast)
Inhibition of apoptosis (the natural process of cell death)
This means that cells within a fibroid keep dividing and refuse to die off when they should, leading to unchecked growth. It’s like the fibroid becomes a self-sustaining ecosystem, insulated from the body’s normal regulation.
This has been shown in multiple studies, including those from Nature Reviews Molecular Cell Biology, revealing that mechanical stiffness can profoundly change how cells “think” and behave.
Again, this raises an important question… if the physical environment of your uterus is driving this abnormal behaviour, is removing the womb the only option? Or is there a better way to restore balance?
Inflammatory & Hormonal Influences
Of course, we cannot ignore the role of oestrogen and progesterone. These hormones stimulate the production of ECM components, including collagen. That’s why fibroids typically grow during reproductive years; when hormone levels are high and shrink after menopause, when hormone levels drop.
But here’s where it gets even more interesting: inflammation, often driven by diet, stress, environmental toxins, or gut imbalance, sensitises tissues to hormonal signals. This means that even normal levels of hormones can trigger abnormal responses in a chronically inflamed body.
So it’s not just hormonal imbalance and more about the context in which those hormones are operating.
Which leads to a question few practitioners ask: What is causing the hormonal and inflammatory imbalances in the first place?
So… Why Aren’t We Told Any of This?
These are published studies, peer-reviewed, and widely accepted in scientific literature. So why is this information not being shared with women?
Could it be that we’ve become too reliant on symptom management, drugs, surgery, or suppression, without asking what’s really driving these issues at the cellular level?
The fact is, our body is brilliantly designed to self-heal, provided it has the right support, understanding, and internal environment.
And that’s where the real work begins, not just masking symptoms, but completely understanding the terrain of your body to find out exactly what’s happening. When you understand the deeper problems, you stop seeing fibroids as womb invaders. You’ll start seeing them as messages from your body; messages that you can respond to.
It’s not about fighting fibroids. When you truly know what your body is trying to tell you, rather than battling with it, you begin listening to it, understanding why it's happening, and begin restoring harmony at the cellular level.
What do you think?
Were you ever told about the role of collagen, ECM dysfunction, or growth factor signalling in fibroids? Were you led to believe they were simply genetic or inevitable?
Drop your thoughts in the comments, I’d love to hear from you.
If you enjoyed reading this, you will love these:
Fibroids: Are They Really Dangerous?
The Lymphatic System’s Hidden Role in Fibroid Growth
The Real Reasons Your Body is Growing Fibroids
This space is where I teach the deeper truths about fibroids, womb health, and healing: the things women are never told. Stay connected as I continue to share the frameworks, insights, and root‑cause teachings that shape my work.
References
Okolo, S. (2008). Incidence, aetiology and epidemiology of uterine fibroids. Best Practice & Research Clinical Obstetrics & Gynaecology, 22(4), 571–588.
Ciavattini, A., et al. (2013). Uterine fibroids: pathogenesis and interactions with endometrium and endomyometrial junction. Obstetrics and Gynecology International, 2013, Article ID 173184.
Walker, C. L., & Stewart, E. A. (2005). Uterine fibroids: the elephant in the room. Science, 308(5728), 1589–1592.
Parker, W. H. (2007). Etiology, symptomatology, and diagnosis of uterine myomas. Fertility and Sterility, 87(4), 725–736.
Malik, M., Norian, J., McCarthy-Keith, D., Britten, J., & Catherino, W. H. (2010). Why leiomyomas are called fibroids: the central role of extracellular matrix in symptomatic women. Seminars in Reproductive Medicine, 28(3), 169–179.
