Copper, Iron, and Endometriosis: Why Supplementation Requires Caution

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

I like to respond to this comment copper helps iron get to where it needs to go so shouldn't women with endometriosis and adenomyosis take copper with their iron and at first that sounds completely logical because copper is absolutely involved in iron metabolism copper is required for enzymes like ceruloplasmin and hephaestus which help convert iron into the form that transferrin can transport throughout the bloodstream. So if you stop the conversation there adding copper almost sounds like a great idea but biology isn't that simple because you can't look at one pathway without looking at everything else that metal is doing inside the disease and that's exactly where this argument begins to fall apart let's start with the biggest misconception the problem in endometriosis is generally not that women can't mobilize iron because they're copper deficient the real bottleneck is inflammation chronic inflammatory cytokines especially IL-6 stimulate the liver to produce hepcidin hepcidin is the master regulator of iron when hepcidin rises it binds to ferroportin the only known iron export channel in the body then ferroportin is internalized and destroyed think of ferroportin as the exit door iron inside intestinal cells can't leave iron inside macrophages can't leave the door is gone.

Now ask yourself something if the exit door has been removed what exactly is copper supposed to do nothing ceruloplasmin cannot oxidize iron that never leaves the cell you haven't solved the bottleneck you've simply added more copper into an already inflamed system. Now here's where things become much more concerning copper is also one of the essential Co factors for one of the most dangerous enzymes in endometriosis LOXL2 if you followed my research you've heard me talk about fibrosis scar tissue adhesions frozen pelvis organs becoming glued together that architecture doesn't build itself LOXL2 is one of the master enzymes responsible for creating it its job is to cross link collagen to stiffen tissue to stabilize scar formation to reinforce extracellular matrix.

And here's the critical part LOXL2 cannot function without copper the enzyme contains a highly specific copper binding site without copper it remains largely inactive with copper it begins cross linking collagen fibers into dense permanent scar tissue. Now think about what happens in endometriosis the lesions already overexpress LOXL2 they're already trying to remodel tissue they're already creating fibrosis they're already building adhesions. So if you introduce additional copper what have you potentially done you've supplied additional cofactor to one of the enzymes driving the disease architecture itself.

In other words you're trying to improve iron transport by feeding an enzyme responsible for making the disease mechanically worse. In other words you're trying to improve iron transport by feeding an enzyme responsible for making the disease mechanically worse that's like pouring gasoline onto a fire because you wanted the smoke to clear copper helps stabilize HIF-1 alpha and promotes VEGF signaling those pathways stimulate new blood vessel formation so now copper isn't only helping fibrosis it may also be helping lesions establish and maintain their vascular network copper helps stabilize HIF-1 alpha and promotes VEGF signalling those pathways stimulate new blood vessel formation so now copper isn't only helping fibrosis it may also be helping lesions establish and maintain their vascular network and that's not the end of it copper is also a redox active metal just like iron it can cycle between oxidation states.

That means free copper can participate in Fenton like chemistry producing highly reactive hydroxyl radicals those radicals damage DNA lipids proteins mitochondria. Now remember the iron paradox we talked about in the previous video the lesion already exists inside an oxidatively stressed environment adding another redox active transition metal into that system may increase oxidative pressure even further. And here's the irony the lesion appears remarkably good at surviving oxidative stress healthy tissue not so much the surrounding tissue the ovary the pelvic nerves they're the tissues that often pay the price high copper intake can reduce zinc availability.

Why does that matter because zinc supports antioxidant defenses and multiple studies have shown that women with endometriosis already tend to have an elevated copper to zinc ratio and that ratio actually correlates with disease severity so supplementing copper doesn't simply add copper it may push that imbalance even further. Now here's what really convinced me researchers didn't decide to study copper supplementation as a treatment for endometriosis they studied the opposite copper depletion using copper chelator like tetrathiomolybdate and what happened fibrosis decreased inflammatory cytokines decreased collagen deposition decreased pain related pathways decreased lesions became less aggressive think about that researchers are actively investigating whether removing available copper slows disease progression meanwhile we're recommending adding more of it those two ideas don't fit together.

Now does this mean copper is bad no copper is an essential trace mineral if someone has a true documented copper deficiency that deficiency absolutely deserves appropriate medical treatment but that's a completely different conversation the question isn't is copper important of course it is the real question is should women with endometriosis or adenomyosis routinely add copper simply because they're iron deficient based on the molecular biology I don't think that's the right target because the problem isn't a lack of copper the problem is inflammation hepcidin ferroportin destruction iron sequestration and a disease that appears remarkably efficient at hijacking trace metal biology if we want to improve iron status our focus should be on understanding why iron is trapped why bleeding continues why inflammation remains high and why the disease architecture keeps expanding adding more cofactor to an enzyme that is already driving fibrosis doesn't solve the disease that simply may help the disease build itself more efficiently and that's why I believe copper supplementation in endometriosis deserves far more caution than it's currently getting.