A Discussion on the Copper Insufficiency Hypothesis, with Morley Robbins
Could lack of bioavailable copper be fueling your iron issues? That’s Morley Robbins’ take, based on 10 years of self-study in mineral research. You’ll learn why iron supplementation may not be a quick fix and get a protocol to optimize your copper levels. We have a reasoned dialogue on what the research may imply and where further study is still needed. Morley also shares results he’s seen with those who have used his protocol. (Tip: favoring whole, nutrient-dense foods—like organ meats and oysters—is one safe way to start getting your health on the right track.)
Dr. Michael Ruscio, DC: Hi, everyone. Welcome back to Dr. Ruscio Radio. This is Dr. Ruscio. Today I’m here with Morley Robbins and we’re going to be talking about a different take on iron, copper, and minerals. I was given Morley’s name from Allison Siebecker who had recently heard one of his presentations, found it very interesting, and thought it might be something that we would all enjoy digging more into. So here we are. Morley, welcome to the show.
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Dr. R’s Fast Facts Summary
Why is Iron important?
- Helps with the production of red blood cells which help carry oxygen and nutrients
- Fatigue, brain fog, exercise intolerance, poor endurance, poor circulation, and feeling cold, can be a byproduct of iron insufficiency
- There has not been any testing or research to compare outcome data using iron supplementation and copper supplementation
Why is copper important?
- Needed for many enzyme functions
- Can’t create ferritin without copper
- Inadequate copper creates hemosiderin
Protocol for copper optimization
- 12-marker assessment + hair mineral assessment + Ceruloplasmin
- Minerals, vitamin complexes and nutrient-dense foods
Food sources of copper
- Organ meats such as liver (beef liver is optimal)
- Cod Liver oil
- Oysters (canned are ok)
- Shiitake Mushrooms
- Bee pollen
- Whole food vitamin C by Innate Response
Learn more about Morley Robbins
- Get help using this information to become healthier.
- Get your personalized plan for optimizing your gut health with my new book.
- Healthcare providers looking to sharpen their clinical skills, check out the Future of Functional Medicine Review Clinical Newsletter.
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Morley Robbins: Well, thank you so much. I’m delighted to be here and I’m looking forward to our exchange.
DrMR: Same here. Tell people just in brief what your background is before we launch into the dialogue.
MR: Quick thumbnail sketch. Pre-med retread, didn’t get into medical school. Did what most guys do when they can’t, they become hospital administrators so that they can boss the doctors around. So I did that for 12 years.
I got a business degree before starting that, and became a hospital consultant. Did that for 20 years and really focused on forecasting. I was pretty good at it, and was fascinated at why everyone was so sick.
So late in life, in my mid-50s, I decided to take training to become a wellness coach and then trained myself in minerals. I’m self-taught, I don’t have formal education, although I’m proud to say that for the last 10 years I’ve read between two and a half to three hours every morning for 10 years, seven days a week.
I’ve read over 5,000 peer-reviewed articles on just three minerals: magnesium, bioavailable copper and iron. And I pieced it together in a very unique way. It’s in the literature, but you have to know what the dynamics are to begin to put the puzzle together, which I’m sure we’ll talk about.
Could Lack of Copper Be Fueling Low Iron?
DrMR: Let’s introduce maybe your chief hypothesis (at least as I understand it), or one of your chief hypotheses. Which is—and again, feel free to amend this if I’ve got this wrong—that low iron or low ferritin may not be the issue, it may actually be a copper insufficiency that’s causing the low iron. Is that a fair hypothesis?
MR: Yeah, I think that’s a good encapsulation of it. The thing is, what people and what practitioners have not been trained to understand is that there is no copper metabolism and there is no iron metabolism. But there is copper-iron metabolism. They are joined at the hip of a very important protein called ceruloplasmin. It’s arguably the largest protein in the human body. It has six copper atoms inside it. Nothing comes close to its size and activity. I have identified some 24 separate and distinct enzyme functions that this one protein does. One of its most important functions is to regulate the redox status, the reduction oxidation status, of iron. And if that doesn’t happen properly, oxidative stress builds in the body and creates havoc.
It’s actually very interesting, in 1927, Otto Warburg and his assistant, Hans Krebs (Hans Krebs worked for Warburg back in ’26 through 1930) were doing an experiment with birds. They bled birds to the point of near death to see what the reaction was in the blood. They were shocked to learn that there was a three- to six-fold increase in copper enzymes. They didn’t know what they were, they wouldn’t be identified for another 15 years. But they were quite taken aback by that. Then a year later, in the United States team at the University of Wisconsin, there were a series of studies to prove that if you deny an animal of copper in its diet, iron automatically builds in the macrophages of the liver.
So we have this juxtaposition of these two metals, copper and iron. On the one hand, when you take iron out of the animal, copper explodes in terms of its response because it’s trying to mobilize iron and get it back into the system. A year later, we find out that when you withhold copper, iron goes crazy into storage areas.
DrMR: Would that cause a low, let’s say, ferritin? Is that one of the things that will lead to the copper reduction?
MR: Exactly, I was just going to get there. The real confusion on the planet right now is, there’s a distinction between iron in the blood, and iron in the tissue. From 1860 to 1972, any clinician who wanted to study iron status in their patients would do a hemoglobin test. And—you probably know this, your professional peers know this, maybe many of your listeners know this—70% of the iron in the body is in hemoglobin. Less than 10% is in ferritin. But what’s important for people to realize is that the serum ferritin that’s measured in the blood test has nothing to do with the ferritin inside the cells. And we’ll talk more about that.
Iron in Blood vs. Iron in Tissue
The really important point is this dichotomy: iron in the blood is not representative of iron in the tissue. In fact, the iron in the tissue can be up to 10 times higher than the iron in the blood. That’s the pioneering work of Bruce Ames back in 2004.
At one time, he was the most quoted scientist on the planet. At the peak of his career, Bruce Ames was this demigod of physiology at Berkeley.
DrMR: How does one measure tissue, or cellular, iron? Is there a good marker for that?
MR: There are good markers, but they have challenges. The definitive marker is a needle biopsy, which is very painful. And the other is a 2 Tesla MRI, which is very expensive, but it’s now becoming the gold standard for measuring iron status in the brain, eyes, thyroid, heart, pancreas, liver, kidney. For the people who don’t know that there is this dramatic difference between iron in the blood and iron in the tissue, my assertion is… Some people think I’m crazy to say this, but I have a lot of good science to back me up. I’m convinced, Michael, that there is no one who’s truly iron-deficient anemic on this planet.
It is a physical impossibility, when you think about the fact that humans are the most evolved species on the planet and iron is the number one element on the planet at 36%. What we’re supposed to believe is that people who are anemic, wink, wink, can’t metabolize the most important element on the planet. It doesn’t make any sense at all. When you understand the research of Warburg and Krebs, and Dr. Elvehjem at University of Wisconsin, and how important copper is to mobilizing iron and enabling it to be part of the recycling system, then you understand that they are, in fact, inexplicably entwined with each other. And there’s just rampant confusion in practitioner circles because they’ve never been taught that copper and iron are interdependent.
The Importance of Iron (and Copper?)
DrMR: Perhaps for the audience, we should just briefly outline why iron is important. Then we can maybe understand better the importance of how copper can help to optimize iron. I’ll just offer one or two insights, feel free to expand upon this. One of the main things is that iron helps with the production of red blood cells, which carry oxygen and nutrients. So, fatigue, potentially brain fog, exercise intolerance, poor endurance, poor circulation, feeling cold, can all be a byproduct of iron insufficiency.
MR: Again, that’s the party line. And let me sharpen the focus on that.
DrMR: Perhaps copper would be a better way to correct that, but just to give people some context here.
MR: What happens is the internet and doctors’ offices are littered with that mythology. Everything that you’ve just shared is a story, it doesn’t necessarily mean that it’s the truth.
Here’s the way to approach it. You and I have about 5,000 mg of iron in our body. And the female listeners have about 4,000 mg. Let’s just stay with our body. We have about 25 trillion red blood cells. That’s a lot of red blood cells. And when you take the surface area of all of those red blood cells, it’s about the size of a football field (or if you have any international listeners, about the size of a soccer field). So it’s a big surface area inside our body. Think of it, a football field of iron inside our body. And if you put four pennies in the corner—that’s about 90 mg of copper—that’s the amount of copper that’s needed to regulate that football field of iron.
What has happened in the modern era is, people have about one penny of copper in their body because of our food system, our farming system and our pharmaceutical system. There are five key points in making red blood cells that aren’t copper dependent. If you can’t make energy, you can’t make red blood cells. If you can’t make catalase, which is a very important antioxidant enzyme, you can’t make enough hemoglobin. If you can’t run the ferrochelatase enzyme in the heme pathway, which is copper-dependent, you can’t drop the iron into the heme group to be a part of the hemoglobin.
There’s a lot of confusion around that. And in fact, I would argue that every one of the symptoms you just expressed is a clinical sign of copper deficiency, not iron deficiency. And the fact that one of the other popular symptoms is, “Oh, you’re looking really pale, you need more iron.” How do people become unpale? It’s with melanin. And melanin requires tyrosinase in order to properly be formed. Tyrosinase is an enzyme that has a three-sided pyramid with copper at all four points. A lot of confusion about what’s really driving the symptomology. And I think, unfortunately, when there’s low hemoglobin or low ferritin, practitioners are quick to jump on the iron bandwagon.
What the listeners might want to look up is the penetrating research of Robert Hodges from 1978, where he definitively proved—it’s an amazing study—that there’s no correlation between adding iron and having a rise in hemoglobin. But there is an 80% correlation between adding retinol (real vitamin A) and a rise in hemoglobin production. The listeners might wonder, “What’s the connection there?” Retinol activates the gene to make transferrin. And then transferrin is able to participate in this process.
The analogy that I use, Michael, when I’m describing the difference between copper and iron, is iron is like a waiter. About 70% of our iron is carrying oxygen, just as you noted. It’s a very important function. And we live on this planet where we can’t live without oxygen. We also can’t age without oxidants, and for the most part they are caused by iron. Iron is a waiter, carrying oxygen to the mitochondria. And copper is the chef, slicing and dicing the oxygen molecule, activating it, turning it into two molecules of water, to release three ADP that go over to Complex V, so that they can become magnesium-ATP. Then the body can recognize and activate the energy molecule. Until all that’s happened, there is low energy. And you can dump all the iron you want into that system and nothing will happen until copper is there, as the chef, to slice and dice and activate the oxygen.
DrMR: Hmm. A couple of followup questions, coming back to testing for a moment. Has anyone done a correlation with one of the gold standard measures for the tissue levels of iron, either the biopsy or the MRI? I’m assuming that in these studies, they’re running blood panels in tandem, to see if there’s any correlation with blood markers. Has that been done? And if it’s been done, is there anything there to at least suggest that might be a more routinely available corollary?
MR: I have not come across it. I’ve been looking. It’s a great, very thoughtful way of approaching it. I’m not aware of it. I’ve read probably 500 or 600 studies on iron alone, and nothing is immediately coming to mind. What’s important for the listeners to realize is that there are markers that aren’t being routinely measured now, because a lot of people key off of just serum ferritin.
I want to make sure that folks understand what that marker is really about. It is a false flag. There are actually three different forms of ferritin in the body. There is a heavy chain, a light chain, and serum ferritin, and they’re completely different.
The heavy chain ferritin has what’s called ferroxidase enzyme function. Light chain, not so much. What makes the heavy chain work, obviously, is it’s got copper. It’s got access to copper to make that ferroxidase enzyme work. In order to load iron into ferritin inside the cell, it’s essential to have ferroxidase enzyme function. You cannot load iron into ferritin without that enzyme. And if that is not possible, then the iron gets loaded into another protein called hemosiderin. So think of ferritin as an ATM, and think of hemosiderin as a bank vault that requires a manager with a key and a combination to let it out. It’s a very complicated process.
A lot of decisions are being made about serum ferritin. The research goes back to 1976. Worwood and Jacobs, in 1976, were the first to identify the fact that actually the serum ferritin has no iron in it. And then a year later, Paolo Arosio over in Italy confirmed their findings. One of the most definitive studies I’ve seen was by Douglas Kell at Etheresia Pretorius in 2014 talking about ferritin as a very important marker for inflammation.
Those three studies form a compelling platform by which to say that serum ferritin has no iron in it, and the iron has been discharged into the hemosiderin inside the macrophage, and the body is expelling the protein instead of degrading it in the lysosome, the way normal physiology would. That serum ferritin protein is being secreted into the bloodstream is a clear indication of organ pathophysiology. You probably are well aware of the fact that rising serum ferritin is an indication of inflammation. Well, it is, but the iron is back in the macrophages causing chaos. The organ is typically the liver, but it may be other organs, including the heart or the pancreas or the kidney, and then ultimately the brain.
What Are the Data on Copper Insufficiency?
DrMR: So let me zoom aside here for a moment, because one of the ways that I assess the veracity of claims that string together these mechanisms is to see what kind of either inferential data, observational data, or interventional data may help us get a sense for how plausible a given mechanism or inference may be.
One of the things that we could do, it stands to reason, is we could look at how common in the population, in any given population—let’s say, the United States population, just to take one—is iron insufficiency as compared to copper insufficiency. Now, you may not think those to be perfect measures and there may be quarrels with those. But that would be at least one thing we could look at to try to contextualize some of this. Have you looked at those data? And if so, how do these compare?
MR: Well, again, great thinking on your part and great approach. What you have to understand is that so much of the testing is flawed. When we’re looking at iron, there are three different ways to measure iron. We have hemoglobin, which we talked about. We have the serum ferritin, and now we find out it’s empty shotgun shells. Then a third way is serum iron.
When you read the research of Dr. Knutson and Dr. Wessling-Resnick from 2003—a very important study done on macrophages and inflammatory process—they make a very specific point that there is an iron recycling program in the body. I’m going to answer your question, Michael, but I need to have context. There’s an iron recycling program, and every 24 hours, the body needs to come up with 24 mg of iron from the internal recycling system and send it to the bone marrow.
We need another milligram from our diet. One milligram. Not 18, not 36, not 72, or whatever the ridiculous numbers are that are out there. That 25 mg of iron is able to replace 1% of the red blood cells that are dying each day. Every 24 hours, we lose about 1% of our red blood cells. So we lose about 2.5 trillion red blood cells and it takes 25 mg of iron to replace it. In this article by Knutson and Wessling-Resnick, they point out the fact that the serum iron is an indication of how efficient the recycling system is. And they point out that in a woman’s body, serum iron should be about 100 and in a man’s body it should be about 120.
If you look at in a lab range, they’re going to say anything between 35 and 180 is considered okay. It’s not okay and that’s where the confusion is. Then we come to the copper question, which is, how do we measure copper? The most definitive way to measure copper is with an enzyme assay of ferroxidase, which will tell us how many units of this enzyme is expressing in the body that is fully loaded with copper. The serum copper test is a joke. The serum ceruloplasmin is not far behind it. All they’re measuring is the protein assay, not whether it’s working or not.
So you’re basing this mythical or this hypothetical comparison on… the technology is flawed, in measuring both copper and iron. And it’s unfortunate, it’s frustrating. What I’ve done is cobbled together a blood test that begins to interpolate all this and try to make sense of it, But to my knowledge, there is no definitive way of measuring iron in the tissue by a blood test. And there’s no definitive way of measuring copper in ferroxidase in the blood either because the FDA won’t allow it. It’s expressly prohibited. And trust me, I’ve tried on five different occasions.
DrMR: Then if there is not a good answer to that question—which there may not be—the next thing I would move to, if I was trying to grapple with this and reconcile the best approach, would be to look at outcome data. You take people with a symptom, let’s say fatigue, you give them supplemental iron, you give them copper and you compare the results.
One of the things that I try not to get pulled into—and I’ve learned this through my own trial and error—is sometimes a thing looks good on paper on a mechanism level, but it doesn’t shake out when you actually test it. So I try to get an outcome-based read first and then go back to inferring from the mechanism.
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Data on Iron Supplementation
We do have data showing that people improve, fatigue being one measure, when given iron. So that seems to partially violate your hypothesis, but not if there’s also good data showing that copper supplementation helps with fatigue. Although I don’t think copper is going to have nearly the amount of research on it that that iron does.
MR: That’s right.
DrMR: But that doesn’t refute the fact that some people will improve from iron supplementation. So how do you reconcile that?
MR: I think you’re raising a fascinating proposition here. Let me back up a step. I’m going to answer your question again, but I’m going to put it into a different context. So this solar system that we’re a part of started about 11 billion years ago. And according to the astrophysicists, earth formed about four and a half billion years ago. And the life forms that existed on the planet at that time all lived on iron. That was the only source of energy, iron. Then—and I don’t know how the astrophysicists do this, but they say—about 2.45 billion years ago, the phytoplankton started splitting water in the ocean to create oxygen.
There was a point where that amount of oxygen built. It’s called the Great Oxygenation Event. And 99% of life on this planet died, because oxygen and iron is really toxic. What’s fascinating is that on the heels of this Great Oxygenation Event, three things emerged on the planet, copper, multicopper oxidase enzymes—which are a gift to any life form on this planet because those multicopper oxidases have at least four copper atoms, and they’re the ones that can turn oxygen into water, we couldn’t live on this planet if they didn’t do that—and the third thing that formed is cholesterol. It turns out it takes 11 molecules of oxygen to make one molecule of cholesterol, so cholesterol is an oxygen sink.
This copper thing is absolutely essential for working with oxygen. When you’re talking about studies that have been shown on taking iron and people have more energy… they were using arsenic at the turn of the century. We know today that arsenic is not a good thing to use, because it has a downside. And what’s the heavy metal that’s the biggest threat to our well-being? It’s called iron. The body is designed to respond to heavy metals like that by making more hemoglobin. So there will be this transitory burst of energy and oxygenation. Again, more waiters carrying more oxygen, and there is a momentary blip. That’s what the research of Robert Hodges showed in 1978.
DrMR: Let me push back a little bit on that point. And again, I find this back and forth fascinating, because there’s a rich tapestry here of different data points. And it’s interesting to compare rationales. I hope the audience is finding this as interesting as we are.
Soppi, a researcher in Finland, has been looking at hypothyroid women who are non-responsive to thyroid medication. And in one of his studies, in a somewhat controlled manner, he found that getting their ferritin—through iron supplementation—over 100 led to 70% of the women having a decrease in their fatigue, and some other like symptoms.
What’s relevant here to your comment is that it’s not a quick change in their energy. In fact, he finds it takes months until you notice a change in their energy levels. I could understand, and it would be a very valid criticism, if people saw a short blip of energy from iron supplementation. But at least from some of his work, that doesn’t seem to be the trajectory that this follows.
MR: I’ve been looking for that study, so I appreciate your bringing it up. I think it’s important for people to know that anyone who’s hypothyroid has low retinol in their body. There are many pathways in thyroid function that require retinoic acid. The RXR receptor is essential for the thyroid receptor to work.
The markers that are not being measured are: ferroxidase assay, what’s happening to bioavailable copper, we’re not measuring the rise of antioxidants in the body, what’s happening to 8-hydroxyguanine, I think that’d be a really important thing to know, what’s happening to malondialdehyde, what’s happening to lipid peroxidation in these people’s bodies.
I asked Douglas Kell, one of the world’s authorities on ferritin, at the University of Manchester, “Dr. Kell, what’s the ideal ferritin for a human being?”
We were on a Skype call. He looks me in the eye and says, “Zero.”
I said, “Excuse me?”
He said, “You heard me, zero.
“Morley, I want to make sure you understand this. Rising ferritin is not a sign of iron vitality, it’s a sign of organ pathophysiology. Do you understand what I’m saying?”
I said, “Yes, I do.” And I’ve heard about this study by Dr. Soppi for several years. I get really nervous, because we’re back into the world of cholesterol causes heart disease.
For 65 years, Michael, we were held hostage to this moronic idea that cholesterol was the bad guy. When in fact, they forgot to tell us that they started adding iron filings, inorganic iron, in 1941, increased it 50% in 1969. And that, in fact, the iron was causing the problem.
DrMR: Let me add another data point here. I try to keep bringing us back to things that have been measured, just so we have a “prove it” moment. And again, I’m very much open to the critiques here, but I want to keep making this juxtaposition.
I quickly pulled up a study entitled, “Effect of iron supplementation on fatigue in nonanemic menstruating women with low ferritin: a randomized controlled trial.” And the treatment group compared to the placebo group saw about a 20% improvement in fatigue over a 12-week period. It seems to violate logic to assume that iron would be causing this inflammatory damage that would be accompanied by improvements in fatigue. We know from some of the work from Michael Maze that fatigue does tend to, or can lead to, things like depression and inflammatory-induced fatigue.
I guess the question I’m asking is, we have a decent amount of outcome data, supplemental data using iron that tends to work, is there a scenario in which iron supplement can be helpful? How do you account for this? Because the replies, although interesting, seem to be more in the weeds of mechanisms. Are there data, are there trials, where people are using copper and seeing these outcomes in any kind of controlled manner or is it just an inference…
MR: Absolutely, there are. The thing is, we have an industry that funds research. Big pharma funds research, you know that, right? That’s where most of the money comes from.
DrMR: Right, but there’s not an iron medication that pharma is making a bunch of money on.
So we had a conversation recently with Mark Pimentel, and we had a back and forth about probiotics. He was making the claim that probiotics don’t have the same level of research that rifaximin, the antibiotic, does. That I think is a very viable application of your comment, because there’s not the funding behind probiotics that there is for the antibiotic rifaximin. But copper to iron is an apple-to-apple comparison, both non-patentable (for the most part) dietary supplements. I don’t see how pharma makes more on one side of this than the other.
MR: Well, the research is pretty clear that the iron is the mechanism for increasing oxidative stress. Iron is the mechanism for increasing inflammation. I can cite chapter and verse with the studies. You can read the work of E.D. Weinberg at Indiana University. Again, Douglas Kell, amazing research that he’s done.
DrMR: Let’s go into his research. Has he—just as one example, perhaps there was a different study setup—published something where he took people with chronic fatigue, fatigue, depression, something, gave them copper compared to a placebo group and documented a favorable impact?
MR: Nothing is coming to mind, but what he has documented is the absolute devastation that iron has inside the human body. You’re hinging your whole argument on, well, people feel better. Well, first of all, “feel better” is the placebo effect. You just give people a sugar pill and they’ll feel better.
DrMR: Agreed, I think we have to be very careful against placebo. I fully agree with you.
MR: What we need to dig into is the question, is there more ATP being produced? Are there, in fact, less oxidants being produced in the body? Is there, in fact, more ferroxidase enzyme function being produced?
DrMR: Right, I understand that. That’s a starting point of the scientific process. But at some point someone should document that having an appreciable effect in a human being. And until we get there, then this is all just speculation. That’s what I’m trying to get to. If there’s this large body of research, surely someone has taken 15 people, given them some sort of assessment of how they’re feeling pre- and post-, and documented that improvement.
Caution is Required With Iron
MR: I think the person that comes to mind that probably has done the most work to challenge this “iron solves everything,” is Leslie Klevay. He’s a guy who worked at the USDA human research lab in Grand Forks, South Dakota.
DrMR: Sorry, just one thing really quick, more for the audience. I’m not trying to proclaim that iron fixes everything. I think there’s a time and a place to consider supplementation. But yeah, I don’t want to make anyone here think that if you’re tired, just go and indiscriminately start popping iron pills!
MR: I think Leslie Klevay has pulled the curtain back on what copper is really doing in our body. And it’s an “oh my God” moment. Based on his research, there are 80 anatomical, chemical, and physiological defects in our heart that are copper deficiency. He’s done research on neurodegeneration, he’s done research on neuropathy.
I was born in 1952, Michael. I grew up with Geritol. Do you know what the history of Geritol is?
DrMR: I do not.
MR: It was conceived as a way to solve iron-poor blood. And when those ads started to appear on TV, Geritol was taken to court. What’s fascinating is it took 10 years for that lawsuit to work its way through the courts. What’s even more fascinating is to find out what governmental agency actually brought the suit. Was it the FDA or the FTC? It’s a real condemnation of our nation that it was the Federal Trade Commission saying that it was misleading advertising and they had to stop the advertising. But after that decade of advertising, it was locked in the mindset of people around the world, not just in the United States, that “Oh, iron is good if you’re feeling fatigued.”
I have a Facebook following of 175,000 people. I have thousands of people around the world following my Root Cause Protocol. Most of those people have been living a life of anemia and told they were anemic for most of their life, and have been taking iron supplements most of their life. When they finally switched to my protocol, they regained their life. Now, that’s all anecdotal. I don’t have a scientific study to back up my work, but what I can tell you is, I sleep very soundly at night knowing that there are thousands and thousands of people around the world waking up to the vital role that bioavailable copper plays to regulate iron, to allow our mitochondria to do what they’re designed to do, and that makes energy.
What’s increasingly appearing in the research is the role of labile iron—I used to think labile meant free, no, it doesn’t mean free, it means reactive—so what reactive iron does to undermine the efficiency of the mitochondria, undermine the efficiency of the nucleus, undermine the efficiency of the lysosome and every other organelle inside the cell. I can very confidently connect you to iron-induced diseases all over the map. And this idea that we need to somehow prove that iron is going to help people get more energy scares me to be honest, because it’s absolutely false.
DrMR: I share your trepidation about people reading an article online about iron and then saying, “Well, I’m going to go take iron.” I think we should be careful with iron.
MR: Millions do that every day.
DrMR: I think we’re definitely in agreement there. Please do not—just because you heard me mention Soppi’s study about iron—think you should just go out and do that. I would only recommend using iron under the guidance of a clinician, because iron, to your point, can be oxidizing. I think we’re in a little disagreement of how much iron will get you to that point where you start having oxidation or inflammation. But nonetheless, you run the risk. Even if you’re taking my more conservative posture on this, you run the risk of harm through inflammation and potentially other mechanisms if you overdo it with iron. I think that’s a good public service announcement for us to make.
I just want to make one quick remark here and then move into your protocol. I also want to say that certainly if there is ample anecdote, I think something is worth looking at. I’m just trying to run through all these questions. With a new idea, I have a litany of questions that I try to satisfy. There is not always good satisfaction for all those answers, but again, that doesn’t mean that there may not be something there. As I’ve said before on the podcast, I believe in being evidence-based but not evidence-limited. Meaning if we don’t have a robust body of evidence, we can still think outside of that.
Just a really quick remark before we go into your protocol, because I do want to expand upon that. Just to give some background information for the audience, about a 30% prevalence has been documented in what’s known as anti-parietal cell antibodies, or antibodies that damage the lining of the stomach, in those that have thyroid autoimmunity. There’s this immune attack that damages the thyroid and that can lead to a decrease of hydrochloric acid. And that may be what causes some of these hypothyroid women to be at a greater risk for iron deficiency.
I think we’re in disagreement on that point and how you address it, but that’s just a tag there on that point.
A Protocol to Optimize Copper Levels
I’m curious… it sounds like testing this isn’t easy to do. But do you have a protocol that can help rectify this? I’m very curious to hear more about this.
MR: So I cut my teeth in this nutritional work by studying hair tests. A couple of years into it, I realized that I was missing something, and really started with focusing just on magnesium. Then for some reason, my attention was diverted to copper. Then I found out that copper is in two forms, it’s bioavailable or it’s unbound. There’s a lot of confusion in mainstream medicine of all degrees around that, and that this copper is meant to be complexed in this protein and in a whole series of vital antioxidant enzymes: superoxide dismutase, catalase, glutathione peroxidase. There’s a whole series of critical enzymes that are designed to neutralize the oxidants.
I started to work with blood and I started to basically put together a panel. I call it the Full Monty Iron Panel. But I’m looking at all the different iron markers that you and I discussed. I’m looking at percent saturation, serum copper, ceruloplasmin, but also at vitamin A and vitamin D, at magnesium inside the red blood cell. I look at 12 different markers. And what I’ve come to learn is that when the hair test is synced up against that blood test, you begin to get a real pattern of imbalance. You begin to realize that the stress of the individual’s life affects their mineral status. That’s a known fact.
But the greatest stress in the human body is oxidative stress. One Italian researcher referred to the greatest stress in the human body as iron stress. Most people don’t have the courage to say it quite that directly. But the point is, this panel, both the hair test and blood test, helps people to understand where they are from a mineral standpoint.
Then, over the years, I began to focus in on that protein ceruloplasmin, because it really is a true marker for vitality and health. I began to study what undermines its function and what optimizes it. Then I developed what’s called the Root Cause Protocol. It’s basically three key components, minerals, vitamin complexes (not synthetic drivel coming out of test tubes), and nutrient-dense foods that our ancestors used to eat, like cod liver oil and beef liver and foods of that nature.
Take the sugar out of your diet and you’ll lower your iron level, make these other changes that I’ve just mentioned, but then start to introduce more forms of bioavailable copper. The three principles that we work with are bee pollen, whole food vitamin C, and beef liver. It’s noteworthy that the 1934 Nobel prize went to three American Physicians for curing anemia and pernicious anemia with the same product. We know it today as beef liver. That was in 1934, but we don’t eat beef liver anymore because it’s not cache. People don’t like it.
In fact, there’s more copper than iron in that organ meat, and their organs actually do have more copper in them. That’s how our ancestors stayed healthy, because they had sources of bioavailable copper regularly coming into their body to help the body regulate the iron.
The protocol is really designed to reverse the contemporary belief that we need more iron, and this other thought that we need less copper. “Because most people are anemic and they’re copper toxic,” that’s a bold-faced lie. In fact, most people are drowning in iron in their tissues and most people don’t have enough bioavailable copper to spit at. That’s the tragedy of our time, that these two minerals have been misunderstood, have not been studied in tandem. Because I think all the research that you’ve identified, excellent research… let’s bring copper into the picture and see what happens. Completely different set of outcomes, I would argue.
People are able to download the protocol. Go to my website, RCP for Root Cause Protocol (RCP123.org). I give away the answer. We have 100 people a day downloading that manual, and we have a thousand people a week going to Facebook to join the magnesium advocacy group to learn more about this protocol. So I sleep well at night. And I get emails and calls from people all over the world thanking me and saying that I’ve saved them, I’ve cured them or whatever. And I say, “No, you can thank Mother Nature. All I did was connect the dots.”
I think there’s a lot of mythology in nutrition and medicine. I think there’s a lot of confusion. There’s a lot of if-this-then-that. But I think people have failed to step back and really think through, “How does the body really work?” What I’ve found as the breakthrough was going into the research from the 1910s, 1920s, 1930s, 1940s. There’s penetrating understanding of how the body really works, not so much in the present day. I’m very cautious about a lot of the conclusions when I hear about research like Dr. Soppi saying we need to have ferritin over 100, when Dr. Kell says it should be zero. I put my stock and trade in Dr. Kell, because he’s got a lot of literature backing up his position.
I will dive into Dr. Soppi to find out what his rationale is. But right on the face of it, it scares me to death, because millions of women have been trained to believe that. And it’s a bold-faced lie from the research I’ve read, and from the work I’ve done with about 6,000 clients in the last 10 years.
DrMR: Well, certainly, I agree with you that if we get people to eat beef liver and maybe some more of these copper-rich foods. If you do a quick search, you can see many of these are likely foods that people are not eating enough. A couple here would be oysters, and by the way, canned oysters are one of my new favorite foods.
MR: Yeah, absolutely.
DrMR: They’re delicious. Organ meats, spirulina, shiitake mushrooms (another thing I’ve been adding to my cells much more after Mike Nelson told me to broaden out my diet), nuts and seeds, leafy greens. I think that’s a highly tenable recommendation that more traditional foods could be a large step in the right direction. Bee pollen, hadn’t heard of it and that application. But certainly, I wouldn’t think there’d be any downside to having some bee pollen in one’s diet.
MR: You can’t pollinate a flower without pollen and you can’t pollinate an animal without copper. What makes that pollen goldish in color is copper, and the B vitamins that are there. Again, I’m more willing to make inferential leaps. But the B vitamins, as I understand them—and this is not a one and done Google search—are activated by copper and they regulate iron. You begin to get into the physiology and the biochemistry of B vitamins. There’s an amazing connection between copper and iron and the B vitamins. But the hardcore conventional literature makes no reference to copper and B vitamins.
When I was talking to Dr. Kovacs, I said, “What B vitamins are dependent on copper?” He said, “Well, I can’t speak for all of them, Morley, but I can tell you for an absolute fact that folate B9 has an absolute requirement for copper.” Isn’t it interesting that women today have a crisis with folate when they get pregnant? What many of your listeners may not be aware of is that there’s been an 80% loss of copper in the soil worldwide. That’s been documented. That’s not the lunatic ramblings of a guy from Louisiana, that’s an established scientific fact.
People are not aware that high fructose corn syrup blocks copper absorption in the digestive tract. People are not aware of the fact that glyphosate chelates copper down to a pH of one. People are not aware of the fact that many of the antibiotics that are used today cause a 40% drop in copper-based enzymes in the human body. I’ve read those studies. So there’s an all-out war on copper, and there’s this obsession to get more iron into the human anatomy. And it makes no sense physiologically.
DrMR: Morley, what is the whole food vitamin C? Is there a certain product that you’re using, or are there specific foods that are high in vitamin C that you like to have people eat?
MR: Well, the product that I typically recommend is made by Innate Response. It’s a tablet, 400 mg. But there are many foods as you know, that have vitamin C in them.
DrMR: Is it just called whole food vitamin C? Is that the name of the product?
MR: Yeah, exactly. What we have to be careful of is that there are many foods out there that claim to have vitamin C, citrus and a variety of other foods, maca and things like that. What we have to step back and ask ourselves is, do we know how the farmer fed the soil to produce that product? No, we don’t.
What’s important to understand is that the nutrient tables look really cool today. They’ve got a lot of eye candy, but they haven’t been updated for decades. A lot of the conclusions that people are basing their decisions on are based on old data, old research, old food. Universities like Rutgers have done some updates. In the year 2000, they compared the nutrient value of commercial products with organically raised, and it was striking how different those foods were.
People have to be very careful about the conclusions that are drawn. What the manual for the Root Cause Protocol does is it gives people very specific recommendations of what supplements to use and what foods to be looking for, and has helped guide a lot of people in this process.
DrMR: I actually really like this program. Again, I want to voice my support especially for incorporation of these foods that I think are unfortunately just not very in vogue in the modern day diet. I think a lot of our audience, being privy to the paleo-type diet, will understand this. But if you go to the general population and do a random sampling of 100 people, the last time someone ate oysters was probably on vacation (maybe, if then), if they were near the ocean or something. Definitely in agreement there.
The Copper Insufficiency Message
One or two thoughts for you here, that I think could be helpful to push this message out to more people. I understand your reservations with some of the corruption in conventional medicine. But the more I learn about alternative medicine, some of those same corruptions are there. What I’ve come to feel, over the years, is corruption is unfortunately just a human constant, and it’s not beneficial to assign corruption to one area and then shy away from that area because that area is corrupt. It just seems, unfortunately, wherever humans go, there’s going to be some corruption that accompanies that.
I say that because I think there’s a large body of doctors who would probably really want to get behind and champion this message. But some of them may need a little bit more documentation to feel comfortable taking that leap. I would invite you to consider ways that you might be able to document this in such a way where a skeptical clinician or even a scared clinician, who wants to make sure he’s got at least some evidence to cover his work, could utilize that. That’s one thought.
MR: Well, Michael, I really appreciate your comments and your genuine suggestions on how to spread this word. I’ve got 81 posts that are called “posts on iron toxicity,” where I typically will have a half a dozen peer-reviewed articles that I knit together around the subject area. I’ve got five that are just devoted to, “You’re not anemic,” five different ways of talking about it. I’ve got hundreds of podcast interviews and I teach a 16-week online class where I have material that is meticulously footnoted when I’m presenting information.
But I’m very open. I don’t want to sound defensive, because that’s not my intent. I’ve worked very hard to amass this collection and body of knowledge, but I’m very mindful of what you’re saying. I absolutely agree with you, when I say the world of convention, that doesn’t mean that everyone else gets away scot-free. Because I think that there is a lot of confusion even in the world of alternative medicine and in the world of functional medicine, largely because these two metals are completely misunderstood.
If you don’t understand the physiological and biochemical relationship between copper and iron, it doesn’t matter what path you take, what training discipline you’re in and what degree of functionality you’re pursuing. If you don’t understand how oxidative stress is made in the body when those two metals get out of sync, you’ve got a problem.
So I think that’s a very valid challenge for me, to be careful that people don’t think I’m just beating up one side and letting everyone else get away scot-free. I really want to take stock of what you’re saying about presenting this. I work tirelessly trying to communicate this information. And I try to use analogies. This has been a very important conversation because no one has posed the questions that you’ve posed in the way that you’ve posed them. It has revealed a weakness in the research, that there hasn’t been this head-to-head fight yet, that I’m aware of. You’re asking great questions about, “Well, let’s do a bake-off between copper and iron and see who’s going to have less fatigue.” I’ve never seen that.
DrMR: An gosh, that would really… if you wanted to get this message to permeate deeper and deeper into the alternative and conventional community. Even a pilot study there, I think, would do volumes to open doors into some somewhat skeptical minds.
MR: Yeah, bring it on. Again, once we start talking about research like that, you got a couple of hundred grand you can loan me? Because I’ve talked to the research scientists, they would jump at the chance to do it.
DrMR: You know, you wouldn’t need a couple of hundred grand. I’m sure that there’s probably someone in your audience who is a doctor who is doing this, who could just take—this would be a retrospective chart review—the normal patients that they treat. Maybe add a little bit of documentation with pre- and post-assessments, and then they can draw that up as a retrospective chart review. There really wouldn’t be any cost for that. That would be a starting point, but would be something that would help to isolate some of the variables here, that would really support your hypothesis.
This leads me to the second remark I wanted to make. Which is, I wouldn’t be surprised if the benefit here came from people eating all these healthier foods and it may not have necessarily been due to the copper. It very well may be the copper, but that’s one other thing where, if you could help to make that documentation of the utility of the copper… as opposed to, let’s say, Mary Sue eating junk food and now she’s eating organ meats. Certainly, just that change alone, irrespective of nutrient or mineral intake, would be vastly helpful for her.
MR: Yeah, there’s no question about it. When you get into the real depth of what ceruloplasmin does—again, that’s a word that your listeners have never heard before, maybe you’re familiar with it—and when you get into the subtle functions of that protein, it is life-changing, it is transformational. And that protein must have copper in order to work. What may come as a surprise to you and your listeners is to find out that that protein caves in the presence of ascorbic acid. Maybe a topic for another conversation is to delve into that topic alone, about what the spectral property of ceruloplasmin is that gives it its vitality.
It’s an intense blue light. And what does ascorbic acid do? It bleaches it. And we can spend an hour talking about that alone. To me, it’s one of the great travesties on this planet that ascorbic acid is being sold as vitamin C, when it’s not. It’s the pro-oxidant shell of a six-part antioxidant vitamin complex.
DrMR: Certainly another can of worms there that we’re starting to open! I think we’ll leave it there in the interest of time today, but that’s certainly another interesting topic that we can explore.
Are there any closing words that you want to leave people with? And then, would you also please repeat your website and anywhere else you want to point our audience to?
MR: Sure, yeah. I would just caution people to question the social meme that people are anemic and copper toxic. What I’ve learned over the last decade is it’s just the opposite. People who want to learn more about this can go to my website, rcp123.org or they can go to Facebook. It’s a Facebook group called the Magnesium Advocacy Group, MAG. For people who want to reach out to me privately, my email address is email@example.com and my cell phone for those really curious-minded is (847) 922-8061.
The hosts are always like, “You gave out your cell phone number?” I find people are very respectful of my time. I’m pretty busy guy. But when someone calls me, I know it’s important. I welcome those comments and questions. As I say, I’ve never met a question I didn’t enjoy.
And I really appreciate the opportunity, Michael, to have this exchange. I will say it’s been one of the most invigorating I’ve ever had. I really appreciate the thought that you put into it. And I like the fact that you really want to ground the discussion in science and the literature, and be able to have a very healthy dialogue around both.
DrMR: Well, thank you. I appreciate that. And thank you for letting me ask some hard questions. I find it so enjoyable when we can air these different ways of looking at something and come out, I think, with what was a very rich dialogue. Thank you also for taking the time and for sharing your thoughts with us.
MR: Absolutely, and hopefully we’ll have another opportunity to take a bite at the apple.
DrMR: Sounds good to me. Thank you again, Morley.
MR: You bet. Bye bye.
What do you think? I would like to hear your thoughts or experience with this.
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