How Endometriosis and Adenomyosis Can Deplete Usable Iron

Watch the original video on TikTok

Full transcript of the original video, lightly edited for readability.

This is a great key point I'd like to highlight that is supported in my hypothesis. Low iron, the fatigue, the dizziness, the weakness, the shortness of breath, the hair shedding, the feeling like your body is running on empty. There's an actual reason why you're feeling this way. However, a lot of women are told, you're just bleeding too much. Take iron. And, yes, heavy bleeding is a major part of it, but there's more to it than that. I want to go deeper, because in endometriosis and adenomyosis, low iron is not always as simple as you lost blood, so now you need iron.

What I'm finding is that many women may be dealing with an iron paradox. Systemically, the body is iron starved, but locally, especially around endometriotic lesions, the pelvic environment can be overloaded with iron, hem and oxidative stress, a pathological process taking place. So the woman feels depleted, exhausted, and anemic, while the disease environment itself may be sitting in a toxic iron bath, robbing the body. That is the paradox. A local iron overload versus a systemic iron deficiency. Low iron in the blood, high iron stress around the lesions.

And that connects directly to my hypothesis. My research framework argues that endometriosis may survive through a selective redox survival state. In simple terms, the lesion may preserve just enough antioxidant Protection to avoid death, while still keeping enough oxidative signalling active to drive inflammation, blood vessel growth, fibrosis and survival. Now, let's Connect that to iron. Endometriosis and adenomyosis can lower iron through two major routes. The first route is obvious blood loss. Women with adenomyosis especially can have extremely heavy, prolonged, clotted bleeding.

Endometriosis can also come with heavy menstrual bleeding, spotting, and inflammatory cycle disruption. Every cycle, blood leaves the body. And with blood, iron leaves the body. Over time, that can drain ferritin, lower hemoglobin, lower transferrin saturation, and create real iron deficiency. But there is a second route that is less obvious. Internal bleeding. Endometriotic lesions can bleed cyclically. Endometriomas are literally filled with old, degraded blood. That is why they are often called chocolate cysts. That blood is not leaving the body through a normal route.

It is trapped. The red blood cells break down, hemoglobin breaks apart, heme is released, iron is released, and the pelvic immune system has to clean it up. That job falls heavily on macrophages. Macrophages engulf red blood cells and heme. They try to contain the mess. But when there is too much bleeding, too much heme, and too much iron, those macrophages can become iron loaded. They turn into what are called siderophages. Basically, iron stuffed macrophages. And this is where the iron trap begins.

Instead of iron being recycled efficiently back into the bloodstream for healthy red blood cell production, it can become trapped inside macrophages and inflammatory tissue. So now the body has iron, but not in the right place. The bone marrow needs iron to make red Blood cells. The muscles need iron for oxygen use. The brain needs iron for normal energy and neurotransmitter function. But the iron is being lost through bleeding and trapped in inflammatory compartments. That is why some women can feel iron deficient even when ferritin looks confusing or falsely normal.

Ferritin can rise with inflammation because it is also an acute phase reactant. So a woman may be told, your ferritin is fine while her transferrin saturation is low. Her symptoms are obvious, and her body is functionally iron starved. Then comes hepcidin. Hepcidin is the master iron control hormone. When inflammation is high, especially through signals like IL-6, the liver can increase hepcidin, and hepcidin shuts down ferroportin. Ferroportin is the export door that lets iron leave intestinal cells and macrophages. When hepcidin rises, that door closes.

So iron absorption from the gut drops, iron release from macrophages drops, and the body enters a functional iron deficiency state. This is why some women take oral iron and feel like nothing changes. It may upset their stomach, it may constipate them, it may worsen gut symptoms. But if hepcidin is high, the body may not be absorbing or mobilizing that iron well. So again, the issue is not just intake, it is regulation. Now, here's where my hypothesis connects. The pelvic lesion environment is iron rich.

Iron reacts with hydrogen peroxide through the Fenton reaction and produces hydroxyl radicals, some of the most damaging oxidative molecules in biology. That Should kill cells. That should push endometriotic cells into ferroptosis, which is iron driven cell death. But the disease does not die. Why? Because the lesion may up regulate survival Shields. One of the key Shields is GPX4. GPX4 protects against lipid peroxidation and ferroptosis. So in my model, the lesion survives because it protects itself from iron driven death, while still allowing enough peroxide signaling to keep the disease active.

That is the selective redox survival state, damaging everything else around it. The cell avoids death, but keeps the danger signals. It resists ferroptosis, but keeps oxidative pressure. It may be creating this environment. Why? Because it can survive iron toxicity while using that toxic environment to drive inflammation, angiogenesis, fibrosis, and epigenetic change. That is why this is so important. Low iron in women with endometriosis is not just a nutritional issue. It may be a disease architecture issue. Heavy bleeding drains iron, internal bleeding traps iron.

Macrophages hoard iron. Inflammation raises hepcidin. Hepcidin blocks absorption and recycling. The bloodstream becomes iron starved. The pelvis becomes iron toxic. And the lesion survives by building resistance to the very iron driven death. That should eliminate it. That is the breakthrough concept. The woman is depleted, the lesion is adapted. The body is trying to contain damage, but the containment system becomes part of the disease loop. This may help explain why women feel exhausted even when doctors say their labs are not that Bad.

It may help explain why oral iron does not always work. It may help explain why adenomyosis patients can become so severely depleted from heavy bleeding. It may help explain why endometriomas are so inflammatory and damaging to ovarian tissue. And it may help explain why targeting iron biology, ferroptosis resistance, macrophage sequestration, hepsin, and redox balance could become a major future direction in endometriosis research. If you suspect low iron anemia, heavy bleeding, or severe fatigue, you need proper labs and medical care. But the bigger message is this.

Women are not tired because they are weak. They are not exhausted because they are dramatic. Their bodies may be stuck in an iron war. One side is losing iron through bleeding, another side is trapping iron through inflammation. And the disease may be surviving by adapting to iron toxicity instead of dying from it. That is why I keep saying endometriosis is bigger than all of the reclassifications it keeps seeing. Estrogen, immune, insulin. And this right here is where I believe the future of endometriosis is going.