Regenerative Health with Max Gulhane, MD
I speak with world leaders on circadian & quantum biology, metabolic medicine & regenerative farming in search of the most effective ways of optimising health and reversing chronic disease.
Regenerative Health with Max Gulhane, MD
51. Morley Robbins: Copper, Iron and Trace Minerals for Optimal Mitochondrial Health
Morley Robbins is an expert on the role of trace minerals in health. In this episode we go deeply into the biochemical mechanisms of copper and iron use in the body, particularly how they relate to mitochondrial health.
We finish with a discussion about soil mineral depletion and the effect of agricultural herbicide glyphosate in chelating copper, reducing its prevalence in the food supply. This is quite a dense and technical interview, but presents a fascinating different perspective on the mitochondrial approaches of Dr Jack Kruse and Dr Laszlo Boros.
TIMESTAMPS
0:02:21 Podcast begins
0:18:25 Mitochondria, Melatonin, and Copper
0:33:31 Copper and Energy Regulation Role
0:42:04 Copper and Iron's Role in Metabolism
0:55:45 Iron Dysregulation and Role of Ferritin
01:01:49 Iron and Copper Dysregulation Explained
01:17:19 Copper Deficiency and Industrial Herbicides
01:30:25 Minerals and Health Impact Exploration
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In today's episode I'm speaking with Morley Robbins. He is a former hospital consultant turned self-taught expert on the role of trace minerals in health. He strongly advocates for identifying and correcting mineral deficiencies as a strategy to optimize health. In this episode, we go pretty deep into the biochemical mechanisms of how the body uses copper and iron, and particularly how they relate to mitochondrial health. We finished with a discussion about soil mineral depletion and the effects that monocropping, including the widespread use of the herbicide glyphosate, is impacting the chelation of copper and therefore reducing its prevalence in the food supply. This interview is quite dense and quite technical, but it was very interesting to get Morley's opinion on things, and we I cross-referenced his point of view with a lot of the guests that I've had on previously, including Dr Jakuz and Leslie Boros. So have a listen, tell me what you think and I hope you enjoy it and I'll see you in a minute. I'll see you in a minute, bye, bye, bye, bye. So, morley Robbins, thanks for coming on. The Regenerative Health podcast.
Morley Robbins:Max, I'm thrilled to be here and look forward to our discussion.
Dr Max Gulhane:So give the listeners a background on yourself and how you arrived at exploring this amazingly interesting world of minerals and how they affect human health.
Morley Robbins:I grew up in a very sickly family here in the States. The mom was an alcoholic and dad was manic depressive schizophrenia and my sister became a nurse and I was supposed to become the doctor and fate got in the way. I found out I wasn't a good student but I went into hospital management and then consulting, did that for 32 years and developed frozen shoulder from pulling a suitcase behind my back for 20 years through airports, hither and Yon, and friends at a health food store told me to go see Dr Liz. Well, I knew that was a chiropractor and I said I don't do witchcraft. Well, dr Liz is now my wife and she's the one who introduced me to natural healing and she sparked this interest in me around understanding the innate healer.
Morley Robbins:I'd never heard that phrase. In 32 years of working in hospitals and I'd had thousands of conversations with doctors, I'd never heard that phrase innate healer. But if there's an innate healer, why do we have all these doctors? You know why do we need doctors. And so I took it upon myself to really delve into the world of metabolism and, as you probably know, wrote a book called Cure your Fatigue, because what most people don't know is that every symptom in the Merck manual and there's 32,000 of them that are profiled. Every one of them begins with cellular energy deficiency, and that's a really important concept for people to realize is that if the mitochondria start to wobble and can't do their work, they do more than just make ATP. They're incredibly active organelles, as you know. But if the mitochondria go well, then there goes the I guess, the intelligence of the cell, and that's really been my area of focus.
Dr Max Gulhane:Interesting and this concept of the innate healer is I understand what you're saying is one that is very much sidelined or not profiled throughout medical orthodoxy, throughout doctors' education, throughout treatment guidelines. It's sidelined for prescriptions for surgeries, for various types of interventions, and I mean that's another whole conversation in itself. But there's a reason why these structures exist and profit is made on not promoting the innate healer within each and every one of us. But let's start with mitochondria, because this is a topic that I've been very much leaning into over the past six months, and regular listeners to my podcast have heard from Dr Jack Cruz, We've heard from Dr Lazlo Boros, a range of other guests, and I really think that putting the mitochondria at the center of our disease paradigm kind of gives us the most explainability for these so-called complex diseases like neurodegeneration, cancer, autoimmunity and metabolic disease, and there's so much to be said about it.
Dr Max Gulhane:But really, basically, there's this bacteria that got simply enslaved hundreds of a billion years, billion and a half years ago, and then subsequently make energy for us in a symbiotic relationship. So, as you mentioned, they do a lot more than make ATP and, critically, they make water, metabolic water that is deteriorated amongst a range of other facets and they're obviously receiving light frequencies. So talk to us about how you think about mitochondria in the context of all your research and all your work.
Morley Robbins:Yeah, Well, it's important to put the word purple in front of bacteria. They're purple bacteria. There's a color to their existence. And how do we get the color purple? Oh, it's a blending of red and blue. So when you get into the mechanics of the mitochondria and you begin to explore the electron transport chain, so there's four complexes there, and then, when that's working with complex five, you have what's called oxidative phosphorylation. As you know Well, complex four is the critical step, and we live on a planet that has 20% poison in the air.
Morley Robbins:It's called oxygen and it's not our friend. It really isn't. It's a very toxic element, and the reason why we're here, the reason why you and I are having this conversation on these very fancy devices talking to each other thousands of miles away from each other, is because higher intelligence requires higher levels of energy that were made possible by the harnessing of oxygen to burn fuel. Right, that's. Those are the fundamentals, but the part that people seem to gloss over is that there can be no life on planet Earth without copper. It's impossible. It is the only element on the planet that can regulate iron and oxygen at the exact same time and not create static. And everybody misses that, and you probably know about the great oxygen event 3.4 billion years ago. Right? Who came to our rescue? Cyanobacteria, right, cyanobacteria, blue bacteria. Cyan was a it's very important to know the colors. So cyanobacteria started playing with the sunlight and releasing oxygen because they were engaging in photosynthesis. So it's exciting that you've talked to Jack Cruz.
Morley Robbins:But it's important to recognize that there's three steps to photosynthesis there's photosystem 1, there's photosystem 2, but there's a step in between. Did you know that Plastocyanin? Plastocyanin is the critical step and it turns out that photosystem 1 occurs second. It was discovered first. That's why it has the Roman numeral 1. But photosystem 2 is the first step, Moves the electrons to plastocyanin and plastocyanin moves the electrons to photosystem 1.
Morley Robbins:Plastocyanin does not work without copper. Therefore photosynthesis does not work without copper. Therefore you can't release oxygen into the air without copper. But the catch is you can't turn that oxygen into two molecules of water without proper copper concentration in complex 4. And so it turns out that complex 4 is a two-stroke engine. There's a downstroke that creates hydrogen peroxide, h2o2. And there's an upstroke that turns that H2O2 into two molecules of water. So what are the mitochondria? They're water wheels. They're water wheels. And I see the whole deuterium issue a little differently, because I think that it's a sign of defective copper concentration.
Morley Robbins:One of the great copper researchers, paul Kobine. He's at Auburn University. He's originally from Canada, saskatchewan, canada, did his doctoral work there and then became a professor at Auburn University. Guy's brilliant. But in 2004 and in 2006, he's the guy that figured out, based on a yeast model. Yeast are many mammals it's a very cool concept. Their metabolic structure and activity is identical to mammals. It's a lot smaller and, based on his model, he discovered that there's 50,000 atoms of copper in the matrix of the mitochondria and the complex 4 that we're talking about, where oxygen becomes two molecules of water. That complex is blue, sky blue, and that's really important for that complex to work by Red light.
Morley Robbins:Oh, there we go.
Morley Robbins:So what does blue tissue do?
Morley Robbins:It attracts red light and the mitochondria love that red light.
Morley Robbins:People swear by their red lights and their red lasers, not knowing that all they're revealing is that they're copper deficient, because what's the frequency of red light?
Morley Robbins:Oh, it aligns perfectly with the frequency of copper. What's the frequency of blue light? Oh, it aligns perfectly with the frequency of iron. So you hear these two metals opposing each other, expressing different forms of light and it's absolutely amazing that I think a kindergartner could understand this better than a physician, because they understand colors and they think differently, and I think the phrase that I use and I didn't say that to punch you in the nose next it's just most physicians don't know how energy is made. Most physicians don't know how blood is made, and this is the fundamentals of our metabolism, and it's important that the way I approach it is ignore the enemies, the pathogens and the toxins and the heavy metals. Let's ignite the energy. That's what this is all about, and I think that aligns with your desire is to help your clients increase their metabolic profile so that their machinery and their messaging, their signaling, can be at an optimal level.
Dr Max Gulhane:Yeah, for sure, and I'll give you the lessons, a bit of a background about that Great oxygenation event. And the point that you brought up, molly, was that the world was an incredibly unhospitable place back those three billion years ago. It wasn't conducive to life as we know it existing, and that those cyanobacteria essentially existed in the oceans. They used their harness solar energy to produce oxygen as a biproactive photosynthesis and they bubbled along for so many billion years that they eventually changed the content of the atmosphere. So the dynamics, the nutrient dynamics, change so that we're able to evolve. This oxygen-aerobic metabolism was able to evolve. So that's a very interesting point.
Dr Max Gulhane:And what you've talked about in terms of the specific role of copper in the electron transfer chain in the mitochondria is also fascinating Because, as you've given us an overview, we can't do these fundamental processes, which is photosynthesis, and oxidative phosphorylation is a reversal of photosynthesis.
Dr Max Gulhane:I think I'll hammer that point on Because photosynthesis is taking light and it's taking water and it's turning that into basically sugar, essentially carbohydrate chains, and what we do when we burn substrates in our mitochondria is we're taking the chains of hydrocarbons and we're taking oxygen and the outcomes is water and CO2.
Dr Max Gulhane:So I also want to emphasize the point that you made, which is that that fourth complex is a red light receiver, and the value or the role of red light therapy. One of them is that it's assisting in the function of the mitochondrial electron transport chain, and I think there's even new evidence that the structured water in the mitochondria is also acting as a chromophore, is acting as a absorber of water. So the question, then I think that's relevant is we're trying to optimize these mitochondrial functions and we're doing so through a light environment. We do so through food substrates into the electron transport chain, and Dr Lazer Boris, who I agree with, advocates strongly for fully grass-fed butter and beef, tallow long chain fatty acids as well as ketones. But what you're proposing is that we can also tune these mitochondrial engines by ensuring adequate amount of these trace minerals. So talk to us about that idea.
Morley Robbins:Yeah, so let's go back to that GOE Great Oxygenation Event, and three chemicals came and saved us. It's really important to understand. So, to get a little technical, there's something called multi-copper oxidases. These are enzymes that turn oxygen into water in one fell swoop. It's actually a four-step process, but they're called MCOs. We have a thousand different forms of MCOs in our gut. Think about that, but it happens like that. So the oxygen becomes two molecules of water at the courtesy of this enzyme. So that was the first really important development. Second, you've probably heard of melatonin, right yeah?
Dr Max Gulhane:of course.
Morley Robbins:It's more than a sleep aid it's a master anti-oxygen.
Dr Max Gulhane:Yeah, go ahead. And it evolved, dandy. That's the point that Dr Russell Reider has made is that it evolved mitochondrial antioxidant capability well before it was a circadian signal or well before it was a sleep inducer.
Morley Robbins:Yeah, and it's the master antioxidant inside the cell. So melatonin is the master antioxidant in the cell, inside the mitochondria. Glutathione is the master antioxidant in the cell and ceruloplasma is the master antioxidant protein in our body. And so there's a real critical requirement to manage this oxygen. And so that was the second chemical was melatonin. And the third is my favorite, that you've heard of cholesterol. Right, it was the third chemical that came on the scene, and it's important to understand that in order to make cholesterol, it requires 11 molecules of oxygen. So the production of cholesterol is in response to copper deficiency. So when you don't have enough copper to metabolize the oxygen, the body has this wisdom to say well, I'm going to store it in cholesterol and we'll begin to make things from this. And so those three chemicals are some of the most important.
Morley Robbins:And so what's happened in the modern world is we don't know anything about the GOE. We think that melatonin is a sleep aid and we don't know that it's being made in every mitochondria of our body, and we have 40 quadrillion mitochondria, and it's distributed unevenly throughout the body. The number of mitochondria in the heart is very different than the liver. It's very different than the neurons of the brain. Some of the neurons have 2 million mitochondria. That's important to know. Especially, like the substantia nigra, where you get Parkinson's, it's an enormously dependent upon functioning neurons in the neurons of the substantia nigra.
Dr Max Gulhane:Yeah, and I'm glad you brought that up, because this idea of human diseases, these complex diseases, diseases that are killing people, so neurodegeneration, heart disease, they are diseases of organs with the most mitochondrial density. And let me add in age-related macular degeneration, because that's, the retina has the highest density of mitochondria and the endocrine system is also quite dense. So if we're thinking about what's killing people and what I see in my GP clinic, what we see in terms of the general medicine inpatient ward, these are all diseases of organs of the highest mitochondrial density. And when you I mean bringing up the substantia nigra, that's an excellent point and that's a whole kind of another topic. We can talk about melanin and neuromelanin.
Dr Max Gulhane:But the role of melatonin I think of as this kind of guardian of the mitochondrial genome. It's a mitochondrial DNA guardian because it's being made on site to quench this oxidative stress that's occurring as a natural byproduct of oxidative metabolism, and maybe we'll talk about this. Maybe it's a bit of a detour, but the idea of quenching oxidative stress is not necessarily a good idea when these kind of biofotons are also being used in a very, very finely tuned signaling mechanism. So it's not always the best idea to get rid of them all. But I really love it how Dr Robert Fozbrie presented this idea of melatonin in mitochondria and he described a cooling and a lubrication system. The cooling is the melatonin because it's being made on site and the lubrication was the red light because in terms of helping those mitochondrial complexes operate. So let's continue the discussion about mitochondria. I think you're onto a good thing.
Morley Robbins:So, again, the goal is and I think I don't know, that I've ever talked with anyone who understood the link between quote disease and density of mitochondria, so I had soft tea for that. That's a very nice way to describe it, because that's in fact true. And what happens to the mitochondria is they're great recyclers of substrates. They're recycling calcium, they're recycling amino acids, but one of the most important things they need to recycle is called iron. If you hear something you may or may not know and I find this fascinating Scientists and clinicians do not know how oxygen gets into the mitochondria.
Morley Robbins:If I were to ask you, you'd say what's diffusion? No, we're talking about the master pro-oxidant. It's the second most reactive element on the planet After flooring gas. Oxygen is number two. So we're not going to have passive diffusion of a gas into the mitochondria. So it's an active transport. And the people who came the closest were Wittenberg Wittenberg husband and wife team back in 2007. And they threw up their hands and said we don't know how it happens. No one knows how oxygen gets into the mitochondria. The most provocative theory about it is Dr Solis Herrera son man down in Mexico. Have you had a chance to talk with him?
Dr Max Gulhane:I haven't, but I'm culturally aware of his work. Go on.
Morley Robbins:Brilliant guy, and his whole theory is that the melanin is on the outside of the mitochondria and so it's engaging in photosynthesis and releasing the oxygen. Still, I'm not sure that he knows how it's getting in there, but there's this back and forth between melanin and the mitochondrial activity. It's a brilliant model. It makes so much sense conceptually. I think he's still challenged to be able to prove it, but he has a wonderful book on human photosynthesis which is just phenomenal to read. But I think people need to understand that there's some real gaps in our understanding. There's just this well, the oxygen gets into the mitochondria. It's like well, wait, let's start right there. How did that happen? And it's happening at a very fast rate, right? And so the other thing that people, a lot of people, don't know is that everyone puts the electron microscope on complex four. Oh, it's copper dependent. What turns out? The complex one, three, four and five are all copper dependent, and complex two is just an enigma. I don't, we won't go there right now. But the thing is, if one, three, four and five are copper dependent, well, let's talk about that. Let's talk about the fact that the gears of the mitochondria start to grind to a halt. And what? And if the mitochondria can't make heme, that's really where critical breakdown is, as you likely know. And the thing is there's eight enzymes to make heme. Four of them are occurring inside the mitochondria, in the matrix. There's a lot of copper in that matrix, right? So four occurring inside the mitochondrial matrix and four occurring outside the mitochondria, so the ones that end in the word oxidase. It's a pretty good bet that copper's involved, because copper has a unique ability to work with oxygen, to oxygenate and to harness that energy. And that is lost in the world of conventional medicine. Again, I don't think practitioners understand how energy is made and they don't understand the mechanics of what the mitochondria are doing, nor do they understand the signaling. Do you know much about the PAM enzyme? Pam enzyme have you ever heard of that? So there's an enzyme. It's called peptidoglycine, alpha-amidating monooxygenase. It's 35 letters long and max. I get a dollar every time I say it, but it's.
Morley Robbins:There are 4,700 signaling peptides inside our body and what may surprise you is that those peptides are made in the form of parked cars. Does your car in the driveway allow you to get to the store? No, you've got to turn it on right. You've got to start the engine right and the signaling peptides need to be turned on and there's a glycine at the end that needs to be cleaved off and then an amine group is attached and then suddenly the hormone can signal Hormones like insulin, insulin growth factor, you know, just hemopexin, spexin these are things that people have never heard of, and they're all involved in sugar metabolism signaling.
Morley Robbins:That's taking place inside the tissue, inside the cell, inside the mitochondria, and if it's literally when this is on, it works right. You called me yesterday and my phone lit up and I decided to ignore the fact that I didn't know who the phone number was, thank God. But the point is, I got a call, the phone worked and that's great and we were able to come to consensus. But if the tissue can't communicate with itself, if the insulin can't tell all of the other many peptides that it's on the scene, that's what we're up against. And here's the most important part.
Morley Robbins:The PAM enzyme is copper dependent. It doesn't work without copper, why? Because it's working with oxygen monooxygenase, and so I've talked to probably 100 doctors. I've yet to meet a doctor who even knows what I'm talking about, and to me we're at the basis of how the metabolism communicates with itself. Think about hey, we got some incoming, we got something to do, we got. And if they can't get the signal through, if it's just static or if it's an incomplete signal, it's like it's one bar as opposed to five bars, and people aren't aware of that.
Morley Robbins:And so the cornerstone of the root cause protocol is missing. Information equals missing truth. If you don't know that the mitochondria do more than just make ATP, if you don't know that, as you pointed out, that disease is highly expressed in mitochondrally dense tissue, if you don't know that these organelles need to communicate with each other, to me, the mitochondria are the brains of the outfit. The nucleus is just a Xerox machine. And what I really want to know and I'm hoping that you can give me some insight on this who's writing the mitochondria? There's got to be an orchestra leader, right, there's got to be someone saying, hey, we're going to do this, we're going to do that. Who's doing that? I've yet to find the. Is it the hypothalamus? Is it some nucleus within the hypothalamus or I'm just? That's one of my greatest quests to find out Where's the nerve center that's running the mitochondria? Within the cell, within the tissue, within the organ, within the organism. That's the part that absolutely fascinates me.
Dr Max Gulhane:You're raising so many fascinating points, molly, and I will just say what initially just came to my mind in the answer of your most recent question, and it speaks to this idea of centralization versus decentralization. And if we've thought about the model of medical care and science, up till now it's been DNA RNA focused. It's about finding monogenic causes of disease, it's about targeting single gene pathways to solve problems medically. But what I think we're both in agreement about is that this is the stories in the mitochondria and this is a story of decentralization. And it's a story of this decentralized system where we're essentially more worried about our mitochondrial DNA than our nuclear DNA.
Dr Max Gulhane:And if we're taking this centralization and decentralization lens, then I think the answer to your question is that there's not one place in the body. These bacteria, these antibacteria, they're environmental sensors. And when we manipulate the mitochondria to increase their efficiency with light, with red light, with UV light, with different light wavelengths, when we manipulate their function with cold, which essentially reduces the space between those respiratory proteins and increases the efficiency of electron tunneling, when we increase their efficiency with ketone bodies or long chain fats and this is a story of environmental sensing I'm inclined to think that it's ungrounding. We haven't even mentioned grounding the free electrons that you can get, so I would say that they're coordinated in a decentralized way by sensing the environment that they're in.
Morley Robbins:Yeah, and to me, the piece that I've elected to focus on just because it makes the sense intuitively and it's worn out in the research is the bioavailability of copper. Is what ties it all together. One of my most amazing conversations via one of my students down in Australia she's a naturopath. One of her mentors is a. He's a chiropractor of 40 years, a naturopath of 40 years, but he's been an alchemist studying copper and iron for 30 years. It was a fascinating conversation. His name is John and he said you know more lately it would be important for you to know that the copper has a magnetic attraction for light, he went. Well, that makes so much sense when you think about photosynthesis, he said. But it also has a magnetic attraction for ammonia. So what does that represent? Sunlight and ammonia? Well, that's the beginning and end of life. And copper has a relationship.
Morley Robbins:People don't realize that there's four enzymes to break down ammonia. The first is a copper dependent enzyme, and if that obligate enzyme doesn't work right, well, you're going to have a buildup of ammonia and you're going to have brain fog. And where is this happening? In the liver, and there's probably a component of it that's happening in the spleen as well. And the second point is people are not aware of the thousands of activities, enzymatic activities, that are being regulated by the activity of oxygen and iron, by copper hiding behind a curtain. And how do we spell curtain? C-u-r-t-a-i-n, so we can see the symbol for copper, and that's.
Morley Robbins:You made the point earlier. There's no money in a cure. How do we spell cure? Oh yeah, c-u-r-t-a-i-n. And so the basis of the conventional model is on illness, is on lack of energy, and the world doesn't know that. I think it's a very small percentage of practitioners who really understand the way you do that. There's this energy dynamic that's really behind the quote disease dynamic, and that's the amazing work of Douglas Wallace at UPenn, amazing writer and thinker, and if it were up to me I'd give him a Nobel Prize or two for his work so far. But it's just, it's amazing that more people don't know about the central role of energy regulation to drive the whole signaling and all the other dynamics that we're talking about.
Dr Max Gulhane:Yeah, you took the words out of my mouth. I was just about to reference Dr Doug Wallace for the listeners and his seminal work on mitochondria and the bio-energetic, the mitochondrial bio-energetic etiology disease, which is basically giving explanatory power to all these diseases that we're dealing with in the clinic, that the medical paradigm isn't able to provide any kind of useful treatment. And I think that gets to the crux of what you're saying, morley, which is, if you understand the fundamentals of what's going on, then you can reason by deduction to work out what the most effective treatment is. But if you don't understand how the system works, if you don't understand how an engine works, then you're going to be pouring vinegar into the fuel tank instead of fuel. So that's a bit of analogy for where we are.
Dr Max Gulhane:And, before we go into, start talking about the clinical implications and we need to talk. I think we need to talk about these quantum biology concepts and we need to talk about this idea that the proteins and complexes inside the body, the acting, is semiconductors, and no one has talked about this more than Jack Cruz and he's incredibly complex and deep. But there's an idea that these physical quantum properties are occurring within the body. So talk to us about how you integrate those ideas into this copper and kind of mineral centric view.
Morley Robbins:Again, it's about the efficiency of interaction, and you talked about red light being the oil. I've never heard it described that way, but it makes so much sense. It's being able to efficiently harness the light and the energy that is intended to be a part of our cellular structure, and so I think the challenge is a lot of people aren't grounded in mitochondrial enzyme activity. They don't know about the handoffs of electrons and what the enzyme activity is that enables that movement of the electrons, and that, more often than not, those handoffs are made courtesy of copper, the bioavailability of copper and in 1985, earl Frieden, who was then the preeminent iron biologist on the planet. He theorized that ceruleoplasma, which is the master protein, copper protein, was the supply line for the mitochondria. There's this constant sourcing of copper to the mitochondria throughout the body. Well, he was resoundly criticized for that and in 2017, zach Baker proved that he was right. Without a steady supply line, the mitochondria don't work right and the electrodynamics of the mitochondria don't work right.
Morley Robbins:There was a time we've heard of the telegraph wires and the communication that took place with telegraph. The original wires for the telegraph were iron back in the 1850s, and then someone figured out that copper was three times faster to transmit electrons. And so then, suddenly, everyone adopted the copper side. And the way I look at it is what makes a tall building stand still? It's steel girders, right. And what are they made of? Iron, right. But what is it that makes a tall building move? Well, it's copper, because it runs the plumbing and it runs the electricity. And I think it works the exact same way in our body and inside our mitochondria.
Morley Robbins:The way I describe it, max, is that in the world of conventional science and conventional medicine is they love to liken the mitochondria to a kitchen. And every kitchen has a stove, right, and we put a big spotlight on the stove. What's the stove made out of? What's made out of iron, right. And but does the stove, does the stove know what is going to be cooked that day? Does the stove know what temperature the burner should be? Does the stove know what the temperature should be in the oven? No, no, turns out there's actually a chef. I call it a cuisine artist. Well, again, got to spell it right, right. And so no one talks about the cuisine artist inside the kitchen managing and regulating the stove.
Morley Robbins:And it turns out that when you get inside the minority, you get inside complex four, there's he may and he may three. Right, how do you make he may and he may three? Oh, you got to have copper. That's in the literature. It's copper dependent. And so what is he may and he may three?
Morley Robbins:It's actually the stove that holds the oxygen, so the copper can slice and dice it and move the electrons and hydrogen atoms in to enable it to become water, but everyone is fixated on the stove and no one can see the chef.
Morley Robbins:And then the other member of the restaurant that's so important is the waiter. Right, 70% of the iron in our body is a waiter, carrying oxygen, carrying carbon dioxide Right, if we include myoglobin, it's 80% of the iron in the body is a waiter. Well, do we go to our restaurant for the waiter or are we going there for an experience with the food? I would contend that it's. We go there for the chef, not the waiter. And so I think all of the optics and thinking about how energy is made, how energy is regulated, how energy is expended, is more copper centric than anything, because of the very nature of how the process takes place, and I don't think there's enough sensitivity to that in a lot of the discussion is that the physics of the mitochondria is copper dependent Because we're moving electrons, because we're moving photons, and it's a very copper dependent process.
Dr Max Gulhane:The analogy to the building and the electricity transmission really gives me more context and really helps me understand. That makes intuitive sense. Anyone who's touched a copper pipe or a copper spoon. It conducts heat, it conducts electricity that much quicker than those metals.
Dr Max Gulhane:So from a biological point of view it makes sense to me that if we're trying to handle electrons in the most efficient way and that's a great point to make, to hammer home this idea that mother nature is the most experienced and the most expert engineer and she has crafted these organisms over periods of billions of years through the most robust system, which is trial and error and the simple failure of organisms that didn't have the most thermodynamically efficient makeup. So it's a fascinating way to think about it, Molly. So yeah, that's really great. Maybe we can now talk about the kind of clinical implications or try or zoom out from mitochondrial level to kind of whole body and physiology and discuss how copper is regulated, Because the corollary of what you've just talked about to me, and I'm thinking that we need to avoid a Frank total body copper deficiency if we want those mitochondrial function to be optimized.
Morley Robbins:Great point and look forward to the discussion. Now we have to get past the meme that runs the planet. The main, the central meme on planet Earth is your anemic and your copper toxic. And you'd be amazed where that is woven into the thought process of the individual and their practitioner. And the fact of the matter is. The truth of the matter is it's just the opposite.
Morley Robbins:One of the most central paradigms of understanding metabolism is to know that an animal you and I are animals, whether we like it to think of that. But when an animal is denied copper in its diet, iron builds in its liver. That's been well established. It was back to 1928, the University of Wisconsin, dr Hart, steenbach, waddell and Elviem, in March of 1928, proved that. Then, in May of 1928, dr McCarg James McCarg at University of Kentucky, was able to prove that denying copper to an animal caused iron to build in the red blood cell. That's not necessarily good. And so there's this really critical seesaw if you deny copper, iron builds. And we've been talking for almost it's been about 50 minutes. So every second of every day. So 50 minutes times 60 times 2.5 million red blood cells need to be replaced every second In the course of 24 hours, we need to replace over 200 billion red blood cells. That's a lot of red blood cells, but what that's predicated on is the ability to move iron out of the tissue because it needs to be recycled, because it turns out that, believe it or not, it's about 215 billion red blood cells. To replace that many red blood cells, you need 25 milligrams of iron. Average man has about 5,000 milligrams of iron, average woman about 4,000. And that's a lot of iron, especially in a body that's run with just 100 milligrams of copper. So it's a 50 to 1 ratio of copper to iron, or iron to copper. And so here's the most important part, though we need 25 milligrams every 24 hours to replace 215 billion red blood cells, and 24 of those 25 milligrams of iron come from a recycling system called the verticuloendothelial system. I don't think it's taught in practitioner school anymore. I think what doctors are taught is that we need to eat 25 milligrams of iron daily, when in fact, we have this very sophisticated system of recycling the iron, and it's got to get out of the recycling macrophages, principally in the spleen. And if the iron gets stored in the liver, it's got to get out of the hepatocytes, but it's got to be released back into the recycling system to get to the bone marrow to support the production of 2.5 million red blood cells a second. So we're taking 2.5 offline. We're replacing with 2.5 every second. That's really important to understand that. And so 95% of the iron is copper dependent because the recycling macrophages have an iron doorway. It's called ferroportin iron doorway and the iron doorway is run by a copper doorman. That's the work of Giovanna Moussi in Italy, 2014,.
Morley Robbins:Amazing article about the copper driven ferroportin pathway and what practitioners are being trained is that hepsidon regulates ferroportin. Well, hepsidon is a negative regulator. Ferrooxidase is a positive regulator. What's the difference between positive and negative? Positive would be like your mom making sure you get up on time to go to school. Negative regulator would be like a SWAT team coming and grabbing you out of your bed and throwing you into the school. Big difference between those two, right? And so the body runs on positive regulation, unless there's a crisis.
Morley Robbins:When does hepsidon come on the scene? When there's copper deficiency. That's the work of Dr Welch at the University of Utah in 2007. So, again, doctors aren't taught that. And so the very basis of responding to your question you've got to ground your understanding about.
Morley Robbins:Where does copper and iron intersect in the body in order to support the metabolism of the body, and so that recycling of iron that we were talking about earlier, that recycle or the remaking of heme, that's copper dependent too, because you can't put iron into a heme molecule. There's an enzyme called ferrokeletase. Well, guess who's running the Guess who the crane operator is. It's copper. It brings iron and drops it in the center of. Doctors don't know that. So if you don't know the cornerstone of how it's done, then downstream there's going to be a lot of confusion about the mechanics of it. So people need to accept the fact that the meme your anemic and your copper toxic is a lie, when in fact we exist on a planet now where the amount of glyphosate is killing the soil, as you probably know, and glyphosate is a perfect copper chelator. It will chelate copper a billion times faster than it will chelate magnesium. It will chelate copper a thousand times faster than it will chelate iron, and so we can't relate to those numbers.
Morley Robbins:So there was a time, max, when I could run an eight minute mile. I was very proud of that. I was never a great athlete, but at the time when I could run an eight minute mile. My younger son clocked a 402 mile when he was in college and I called him up and said you going to go for it? He said no. He said I could work for months and maybe not shave those two seconds off. But his old man was curious, so I went to a gym to see what it was like to run a four minute mile and I got on the treadmill and cranked it down and was holding on for dear life and then realized wait a minute, the machine's doing all the work. I'm just holding on and almost killed myself trying to get off of it.
Morley Robbins:The thing is we can't relate to a thousand times faster, a billion times faster, because we barely know people who are twice as fast as we are, and so we get lost in the, the bio dynamics of the minerals and these chemicals that we're now exposed to, and the brainwashing that, oh, we need more iron and oh, be careful of that copper, it's going to cause you a problem. We need to flip that narrative and that's why I appreciate the chance to have this conversation so that more people can understand that, wow, there's more to the story and just by way of a parenthetically comment, I renamed what the condition was back in 2020, around April or May of that year. The COV stands for coppers vanished and ID stands for irons dysregulated. And we're back to Hart and McCarg realizing that copper is missing, iron's building, and that's what the research is now showing, what that whole event was all about.
Morley Robbins:And people don't know that. And what does that do to our mitochondria? It kills the mitochondria. They can't. They can't process, they can't engage in their constant activity of recycling and regenerating ATP. And it's just, it's amazing how these fundamental cornerstone facts are not being taught to understand how the higher level functioning of the tissue is dependent upon that process.
Dr Max Gulhane:Yeah, let's to explore that. Molly, I'll make a quick point on the glyphosate before we launch into iron dysregulation. But this idea of glyphosate, when it was brought out, was you know, it's a benign compound, it doesn't harm, you know, it doesn't harm human health, it's all well and good. And it's subsequently been sprayed on you know how many, maybe millions of billions of hectares of land and I want to make quick mention of the episodes where I've talked about glyphosate. So, and the mechanisms of toxicity. So it disrupts the chikimate pathway, which is a enzymatic pathway that we need to make tyrosine, a bunch of other tryptophan, a bunch of other critical amino acids, by nuking our gut microbiome. It's an endocrine, and I talked to Stephanie Seneff about that. It wrecks our deuterium excretion process so we're less able to deuterium deplete our bodies. It acts as an endocrine disruptor after it's chelated probably copper or some other main minerals, and I talked to Dr Anthony J about that it disrupts the exclusion zone water that gets formed on hydrophilic surfaces. So there's so many ways that glyphosate is harming human health and none of them are being emitted by the agricultural companies that make the stuff. None of them are being emitted by government regulators who continue to endorse and push this idea that it's a safe and tolerated chemical and none of these effects are aware of being unknown by clinicians. So I'm glad you brought up the glyphosate and maybe we can talk about that more towards the end of the discussion when we talk about the agricultural implications.
Dr Max Gulhane:But let's dive into iron dysregulation, because you mentioned the effect of iron in COVID. When the pandemic first hit, I was working in COVID wards and emergency department and we were measuring esterine ferritin and it was a hallmark of the degree of inflammation and it was used as a prognostica for who we're likely going to need to be sending to ICU and who we're going to need to be putting on respiratory support. So in that situation the ferritin was, as I understand it was being used as a kind of acute phase reactant, meaning it was a marker of inflammation in the body. Going back to how I see it in my clinical practice, I always interpret it in the context of a seroactive protein which is again an inflammatory mediator, because if it's ferritin is high and CRP is high, it's not giving us a good indicator of iron status. It's simply just reflecting the background information in the body. So talk to us about this use of ferritin as a kind of marker of iron store, as a marker of information, and how you conceive of these concepts?
Morley Robbins:Great. So first we have to understand that there's three different forms of ferritin in the body. There's ferritin heavy chain, there's ferritin light chain and then there's secreted ferritin, and the form that the doctors are focused on is the secreted form. But what they're not taught is that, the heavy chain. Why is it called heavy? Because there's a heavy metal that's running it. What's that heavy metal? It's called copper. So we're back to the ferrooxidase enzyme function running the process of bringing iron into the core. And what's light chain good at? It's good at storing, it's not good at releasing. You've got to have the heavy chain to let it out again.
Morley Robbins:And what happens in the liver is where it's principally. When you see high levels of ferritin, you basically have a breakdown of the liver is taking place and the recycling of the iron, the ferritin, is taking place within the lysosome of the hepatocytes, a really important process. And the lysosome is the stomach of the cell and it's an energy-rich environment dependent upon what. Oh yeah, copper is what's making the acidity rise in the lysosome, and so if it can't complete that cycle properly, the iron gets dumped into the tissue, into the liver tissue, and what gets secreted from the hepatocyte is an abridged form of light chain. It's missing about 10 amino acids and it gets picked up in the blood test as ferritin. But they don't distinguish between the ferritin missing 10 amino acids and the ferritin light chain. They just say ferritin's rising. Well, as soon as you have rising ferritin, you have iron dysregulation, principally in the liver, and so when you have this inflammatory response, the liver is not able to recycle the iron properly.
Morley Robbins:The flip side of it is low ferritin. Everyone knows it Well. Low ferritin means you need more iron. No, it means that the spleen is on the ropes and it's a completely different understanding of what the role of the red pulp macrophages is and their ability to store iron. And the missing piece of the puzzle in low ferritin is hemo-siderin. When was the last time you did a hemo-siderin test of any of your patients? Never, because you were never taught to do that right. So you're taught to do ferritin, but never hemo-siderin. Why is hemo-siderin important? Because it can hold 10 times more iron. It's 10 times more reactive. It's violently effective of the spleen and the liver, both of whom can hold hemo-siderin, but no one ever measures it because they were never taught to measure that. So the thing is that the iron can get dysregulated, it doesn't get recycled properly, it's not able to release its stores. The ferritin is rising because it's being released, because the recycling process is breaking down. Why? Because the energetics and the enzyme activity doesn't support it. And so the rising ferritin is a sign of liver metabolic dysfunction.
Morley Robbins:And no one you knew that hypofaritinemia, the cytokine storm that you were treating in the wards and in the hospital, could have been interpreted as classic raging copper deficiency. But you never had that training. There's a wonderful article that I can send you by a world-renowned MD, phd, leslie Claveille, where he's talking about chronic copper deficiency being at the core of everyone's problem. It was just published, october of last year, and I believe Dr Claveille will be 90 next year, so he's a very active researcher. He's written hundreds and hundreds of articles, but again, the copper side of the story is not known to the public, it's not known to the public's practitioners, and it's really again hiding behind that curtain. And so if you don't know about the curtain, if you don't know about the copper dynamics, you can't understand the iron dysregulation. And so what happens, max, is that far too many practitioners confuse low iron in the blood, in the blood work, and don't think about what that really is.
Morley Robbins:Signaling is high iron in the tissue. The reason why it's high in the tissue is it can't be released to get back into the recycling system, and so there is no blood test that measures iron in the tissue. Everything's in the blood. The only time you can get to the tissue level is to do either a Tesla 2 MRI, which is very expensive, or you can do a needle biopsy of the liver, which is very painful. In both situations, you first. I would love to know how much iron I have in my liver, but I'm not afraid to spend the money or go through the pain.
Morley Robbins:But the point is no one knows about that copper-iron dynamic from the 20s. No one knows that this liver is. It was never designed to store iron. It's designed to store copper and retinol. And what are we taught now? Oh, be careful of copper and retinol, you can become toxic from them, which is like no, that's exact opposite of the truth. And so then the liver has become an iron storage depot, which was never designed by Mother Nature to do that. I mean, it has the capacity the hepatocytes have that natural ability to store iron, but it was never supposed to be dominant function. It was supposed to be storing copper and retinol to support the metabolism of the mitochondria Throughout the body.
Morley Robbins:And the part that a lot of people don't know about is the work of Dr Hammerling in 2016. He'd be a great scientist for you to chat with, because his area of expertise is retinol and how important retinol is to mitochondrial function. And there's something, there's a complex between, or there's a component, we'll call it. It's a structure between complex three and complex four and the electrons turns out. The electrons ride the tail of the retinol to get from three to four and what Dr Hammerling has been able to prove is that it's a lack of retinol that causes the Warburg effect. And it's like wow, that's fascinating and it's interesting. Dr Warburg never coined that phrase. That was actually, I think it was coined in the 80s. But the point is, when did they first know that lack of retinol caused cancer? 1925. Montrose T Burroughs, working at the Rockefeller Institute. He gets his MD degree at Hopkins in 1909. 1925, he publishes an article and four articles in 1926 proving that retinol deficiency causes cancer.
Morley Robbins:Well, what is cancer? What's a buildup of iron and the lack of retinol. The electrons can't flow and you begin to. And the only way to explain the Warburg effect. So the body is designed to burn oxygen in the presence of copper. And in the Warburg effect what's happening?
Morley Robbins:The cells are choosing to use fermentation to make energy Even though oxygen is present. Well, there's only one way to explain why they can't do the oxygen there's no copper, there's no bioavailable copper, and the cancer cells are filling up with iron, which is taking. It's just, it's destroying the availability of copper in that situation. So it's just. It's a wholesale different way of thinking about what's happening inside the cells and inside the mitochondria. But the iron dysregulation is tremendously significant. But people are confusing low iron in the blood work and not aware of the high iron in the tissue. And once you realize that iron can get stuck in the tissue and famous scientists from all over the planet have studied it it's in the literature, there's thousands of articles about it, but that wisdom doesn't make it into the classroom in doctor's school, it's not in the clinical curriculum, and that's where I think the breakdown is in the understanding of the problem.
Dr Max Gulhane:Yeah, A couple of clinical cases to kind of analyze, given it with your frame of reference. So hereditary hemicromatosis is the most common acknowledged kind of clinical setting of iron overload and there's mutations in certain genes that basically people of Northern European descent and the thought being that they evolve in situations of iron, low iron in the environment. And these mutations help us, you know, help these people hang onto iron more efficiently. I have seen heterozygotes of hemicromatosis, so people that carry one mutated gene.
Dr Max Gulhane:They have had ferritins of 500, 600, indicating some degree of iron overload, and then when they go on a very low carbohydrate diet or often a carnivore type diet, so they're eating a heap of steak paradoxically, according to the mainstream and paradigm, that iron overload disappears and the ferritin actually goes back under 300, maybe it goes to 200. So this is a kind of a point that most other doctors and GPs kind of scratch the heads at, because they think that if you're eating very hemoglobin, hemion-rich sources of food, then that will contribute to iron overload. My interpretation of what was going on is that essentially we were fixing a degree of metabolic dysfunction that was dysregulating iron but iron homeostasis. So by what you're saying, it sounds like we probably repleted copper in that nutrient dense animal food diet and that kind of fixed this ferritin number. So obviously the patients lost a heap of weight and they're feeling great. So what's your interpretation of that observation?
Morley Robbins:Yeah, the hemicromatosis is basically a condition of copper deficiency and when we were talking about the PAM enzyme earlier some very important research that I'm going to come back to hemicromatosis in just a second. But there was a husband and wife team, betty Eiber and Richard Mainz, that studied this enzyme for 45 years 20 years at Hopkins and 25 years at University of Connecticut Medical Center. They had funding for 45 years to study this one enzyme. That's a head scratcher right there. But in 2008 to 2012, they were engaged in doctoral research with two of their students and they did a series of experiments with mice and they manipulated the PAM gene so it lowered its ability to express the PAM enzyme. And in another group of mice they withheld copper and got the same level of low PAM expression. So they manipulated the gene, they withheld copper and then in two separate experiments four years apart, they fed copper to both sets of mice and in both experiments PAM expression turned back on, both with the defective genes and with the copper withheld animals. And the student in the second series of experiments his name is Eric Geyer, he's an MD-PhD at Harvard, he's an ophthalmologist and in his doctoral dissertation yeah, I take the time to read those things. It's like it's amazing information in there, max.
Morley Robbins:But he made the comment that heterozygous defects are a sign of copper deficiency. Put it in black and white. And so I think what we to come back to your hemochromatosis topic is hemochromatosis like quote gene defect or is it a mineral deficiency? And to your point, people change their diet. They probably would have responded better to organ meats than to muscle meats because there'd be even more copper there. They might need copper supplementation beyond that. But the point is, the body's not stupid, the body. Think about the wisdom of the body. If we can buy the fact that copper is playing a central role in managing light, managing energy, managing the handoffs and just many, many different things, if it starts to sense that it doesn't have enough copper, it's going to start to change the expression of different genes, and especially those that are handling iron. And so, again, one way to interpret hemochromatosis is well, there's no source of copper. We're going to take this organism offline because we know that if we start to build up the iron, it's eventually going to kill the animal, and that's a rather dark way of thinking about it. But again, I think the body does have this innate wisdom. It says we don't have the requisite substrates to keep energy production. So we're just going to start to change the dynamics and so hemochromatosis will respond to phlebotomy.
Morley Robbins:Very important to get the iron out, get the ferritin out of the system. When I really began to become more sensitive to this whole issue, it was December of 2015. And Dr Liz said you know, you've been talking to a lot of people about iron. He says have you studied yours yet? I went no, don't. So I did a blood test and found out that my hemoglobin was 18.3 and my ferritin was 237. Well, it's a good thing I was wearing brown pants. When I got the results back, it freaked me out, and so that's what I really started to take a deeper dive into understanding this copper iron dynamic and who's on first and what's on second.
Morley Robbins:And the people who understand this the best are the Italian researchers, the Indian researchers, the Icelandic researchers. What do they all have in common? Their countries begin with the letter I. I don't know why, but they just have this awareness about iron metabolism that most don't. But the thing is, it was the copper that was missing in my body that was not allowing the regulation of the iron.
Morley Robbins:Do I have heterozygous genes for this? I don't know. I don't have the courage to do the gene test to find out. I just know I feel pretty darn good with my diet and with the protocol and with the supplementation that I do. I guess if I was a real, true scientist I would subject myself to the gene research to find out. But I take comfort in that if the body is properly nourished the body will express genes properly, because I think that you have genetics epigenetics, because the epigenetics are the environment that are influencing the gene function. But what's above epigenetics, energetics. When the energy is being produced right, it's going to influence epigenetics, which is then going to influence the genes. I think we've become too gene-centric. We need to go back to energy to drive the environment to get the genes to express.
Morley Robbins:Superchromatosis is an enigma in that a heme diet will correct it, but I think you nailed it. You're getting other nutrients in that process. You might also be getting more animal-based fat. The part that people need to understand is that there are two critical pumps that run the copper enzymes. One pump, called ATP7B, makes soloplasmin. The other pump is called ATP7A. It makes all the other copper enzymes. It's amazing what it does, but both of those pumps are activated by retinol. It's actually retinoic acid. It's a hormonal form of retinol. That's buried in the research Cousins and Barber 1987. One little sentence says it all. That is the cornerstone of truth. That's not taught in doctor school is that these pumps need retinol in order to load the key enzymes to regulate the iron, to allow for proper regulation of the system.
Morley Robbins:We live in a fat-free diet now. Most people are afraid of fat. That all started in 1955 when Eisenhower had his first heart attack. Ansel Keys flexed his muscles and said we've got to get cholesterol out of the diet. We can go into all the controversy of that. What they were really doing was eliminating retinol. They knew back in the 20s how important retinol was. It took a generation to be eliminated from our diet. There's just been this gradual erosion of the nutrient density of our food, which I think you understand, and you advocate people going back to a more ancestral diet to get the nutrients that our body is designed to run on. That's really what it comes down to.
Dr Max Gulhane:Yeah, when I'm hearing copper requires retinol to function, I immediately think of the food foods that a code will have, rich source of both copper and retinol. That's liver, that's a ruminant liver. The other enzyme that my listeners will know has a key link to retinol and vitamin A is the photoreceptor system. All of the photoreceptors are bound covalently to retinol. When we're exposed to a whole bunch of artificial blue light, it basically destroys that linkage and causes all kinds of havoc inside the cell. I'll make a couple points about the hemochromatosis. It sounds that, or maybe I'll ask you how can we identify copper deficiency and how can we best replete copper, given what you've said?
Morley Robbins:Just to reinforce what you just said about the retinol the retinol being stored in the liver supports the retinol of the eye. When did they first know about that? Early 1920s. The key is I'm just having a senior moment, Max, I'm sorry. I'm sorry, I didn't make that point. No, I can't remember what question you were asking me. That's okay.
Dr Max Gulhane:I'll also make the point that isotretinol is a retinoid. It's a synthetic retinol. There's evidence that it can interfere with vision in certain patients who take this medication for acne. That's exactly right. There's a finely tuned system here with regard to the body's handling of these enzymes and these cofactors. It's not surprising to me that people could become copper deficient if they're not including nutrient-dense sources of food.
Dr Max Gulhane:They're not including liver, they're not including glass-fed butter, they're not including deep-sea fish, all these important sources of vitamin A. I'm talking about preformed retinol, I'm talking about beta-carotene, or this idea that we can get our vitamin A needs met through plants. It's just not true. Maybe riff on that for a bit more if you could.
Morley Robbins:Sure, in order to restore copper. It's really important. I came across some research just a few weeks ago which was fascinating. I grew up in Baltimore. My nickname is Baltimorely. We bought our dairy from a company called Cloverland. Dairy. Bear with me, max, I'm not a singer, but I want to share this jingle with your listeners Milk and butter and eggs and cheese Fresh from the farm to you, if you don't own a cow, call Cloverland now Northfield 92222. I first heard that, or I first remember hearing that, when I was four years old. That was 67 years ago. That jingle for some reason just got stored. It's critically important.
Morley Robbins:With the article I just found a couple weeks ago Back to James McCarge, 1925, university of Kentucky, he's identifying the foods that have copper. But they also are rich in retinol Whole milk, butter, eggs and the cheese that they're talking about is curd cottage cheese made from curd. How do you spell curd Cu-rd right? Gotta spell it right. And so our ancestors depended upon that basic diet. Daily they were getting exposure to whole milk, butter, eggs and cheese, and then once a week they were eating liver and they were fine Back in the 30s. Back in the 30s, the average intake of copper was 4 to 6 milligrams of copper a day. By the 60s it had dropped to 2 to 5, and now we're supposed to believe that we can get by on 9 tenths of 1 milligram of copper a day. That's a complete violation of the design of our body and the design of our metabolism. So what we're bumping up against, unfortunately, is we buy unprocessed dairy from a farmer about 15 miles from where we live. Milk is not supposed to be white, it's supposed to be yellow. This is beautiful yellow milk and the butter is very rich with. Obviously it's got a lot of beta carotene. Why is the cow important? Because it turns beta carotene into retinol. Thank you, cow, for that. Eggs do the, or chickens do the exact same thing. Eating bugs and grass Turn that beta carotene into retinol. Thank you, little chickens. And people don't know that that chemistry is taking place inside these animals' body.
Morley Robbins:But I think the challenge we've got now, max, is to your earlier points about glyphosate. I'm really freaking out about glyphosate, even within the regenerative farming movement. I have tremendous respect for the farmers who are trying to bring us back to what our ancestors took for granted. But the thing is it's in the air, it's everywhere, it's so pervasive in the soil and it's like there's a wow factor to it and there are ways to correct it. But how many farmers are taking the time and the discipline to make that happen?
Morley Robbins:So I think, the traditional sources of copper. You have to be careful. A lot of people rely on nutrient tables that they go to online. Do you know when those nutrient tables were last updated? It was in the 1950s. They have all sorts of eye candy now. They look really cool online, but the raw data hasn't been changed since the 50s. And so these historical sources nuts, seeds, organ meats, shellfish these were all very rich sources of copper. Do they still exist today? Not in the same way that they did 50 to 100 years ago. And so within the RCP, we're very focused on an ancestral diet. We're very focused on getting the right nutrients. But what we're also realizing? When we first started it, we relied on organ meats as a source of copper.
Morley Robbins:What one of my students did? A very, very enterprising individual. She took the leading brand of desiccated liver and she sent it to a lab to see what the mineral composition was. And, according to the nutrient table, there should be 9 milligrams of copper and 3 milligrams of iron. She got the results back from the analysis, it was reversed there was more iron than copper, and that was sort of a shock to the to the reality of what we're up against, and so it was really once I realized what 2020 was. It was an IQ test, as we talked about earlier.
Morley Robbins:The next year, I developed a in partnership with a nutrient company, formula IQ. I developed something called recuperate, and I think what people need to come to terms with is we do need to supplement copper in our diet beyond the foods and forgive me if I sound like a supplement whore I'm not. What I'm really focused on is people need to get this nutrient, this critical nutrient, back into their metabolism, and we chose to do it in a food-based form. There's desiccated liver, there's spirulina, there's a pinch of tumeric and there's copper, copper bisglycinate, and it's a very bi-available form of copper. I think people need to realize.
Morley Robbins:I've got diabetic clients, type 2 diabetic clients, and I'm sure you have clients who are struggling with their blood sugar. Did you know that blood sugar is a copper issue, that it's when it's rising, there's a lack of copper in the body. You've been trained that it's an insulin issue. Right, it's actually a copper issue. That research goes back into the 30s and 40s and 50s. But the thing is it turns out that children, mankeys, children mankeys' disease are very copper deficient. They're the most glucose intolerant people on the planet. They have no copper and so the copper issue is really central to this blood sugar dynamic.
Morley Robbins:And so people I've got clients who type 2 diabetics taking 5 and 6 of my supplements which have 2 milligrams of copper in them and they have control over their blood sugar for the first time in their adult life. And it's like I didn't tell them to do that. I say take one, maybe two, but many of my clients are now realizing one, they're on their own. It's kind of like this 100th monkey syndrome. There's this vibe out there that we need more copper and they are beginning to get control of their blood sugar, which is then allowing them to wean off of the symptoms of metabolic syndrome. Yeah, go ahead.
Dr Max Gulhane:I would just imagine they're not eating a standard American diet with that copper supplementation. I'm guessing they're eating also a pre ancestral type diet at the same time. Absolutely.
Morley Robbins:Absolutely Important component.
Dr Max Gulhane:Yeah, the point I want to make is that the I think life state is and the wider use of industrial herbicides is this probably one of the biggest impacts on both health and human health and environmental health that no one's talking about. And you know, I think the narrative around environmentalism is kind of has been hijacked to myopically focus on one product which happens to be a waste product of human respiration, where we're turning a blind eye to the destruction of soil microbes, the destruction, the chelation and deprivation of these trace minerals from soil and the consequent effects on the food nutrient density. So, and that's a massive topic, and I think part of the job of my, or one of my hopes with this podcast is to educate farmers and to get them thinking about the consequences of participating in an industrial food system that is contributing to the poisoning of the commons, that is contributing to the commoditization of the food supply and the subsequent, you know, metabolic and nutritional, micronutritional bankruptcy of populations. I think that people can still make the right choice in terms of sourcing from local farmers and I think that is still going to be the best bet, and I would encourage people to maybe do some testing and I think the more access we could have to nutrient testing and things like deuterium, things like iron, things like fatty acid profiles, glyphosate, the better.
Dr Max Gulhane:We could make informed choices and we could even probably guide the agronomist use of trace minerals in the land to therefore increase the nutrient density of the food. If we can identify soil deficiency, then we can then make steps to improve that. My only hesitation with supplementing copper in a supplement form is again is it in context of those cofactors? And two, does it contain deuterium? Have we deuterium depleted that supplement? Because I wouldn't want to kind of be giving people copper which they might need, but also be giving them an extra hit of deuterium that they didn't need.
Morley Robbins:Yeah, that's a fair comment, and I can't speak to the deuterium side. I take a slightly different. I think you alluded to your conversations with Stephanie Seneff, and one of the most riveting conversations I had with her was April of 2018. We were at a breakfast table together and she leaned forward and she said Morley, would you like to know why glyphosate is so hard on copper metabolism? I thought I had died and gone to heaven, but you made the point that there's a relationship between the clearance of deuterium and copper deficiency. I think it's important for people to know that these dysfunctional metabolites may just be an expression of a lack of this critical metal inside our body. I can't speak to what the deuterium status is of that supplement, and that's not the only one. There's copper creams out there that people can use.
Morley Robbins:I think it's important for people to stretch their understanding of how important this mineral is, and there's been a century-long campaign to lower its presence on the planet. It was back to the First World War. They had a lot of armaments they had to get rid of. After the First World War, what did the armaments have? Npk. Oh well, let's turn that into a fertilizer for the farmers, not knowing that that NPK was blocking copper uptake in the root system. That's important to know. That's the genius of soil grass cancer. André Fawcet that book was amazing to read Again, biochemist who was a dairy farmer as a hobby, and he was the one who figured out oh, the soil doesn't have the copper, it's not getting into the milk, it's not getting into my customers and they're getting cancer. That's a really riveting series of connections for people to make that they may not have known otherwise, but he figured that out in the 1950s. And so the thing is that was all pre-pesticides that we're talking about. One of my colleagues told me that glyphosate is actually the ninth most toxic chemical that's used in farming.
Morley Robbins:I'm like what? I can't imagine what the other eight are, and so it's just again. We've got to put it into the context. How is that affecting the microzymal balance, the yeast and the bacteria that are supposed to be communicating with each other, getting the nutrients into the soil, into the root system? Excuse me, and you're absolutely right. We should be doing more testing, both of the soil and the food and the human eating the food.
Morley Robbins:And the testing for copper and iron is at a very rudimentary stage. Max, there are eight tests that you can do to measure the bioavailability of copper. How many of them are barred by the Food and Drug Administration here in the States? All eight. And so we're not supposed to know the bioavailability of our copper, we're just supposed to know that we need more iron, which is that is so pedestrian and ill-informed that people have got to get off this iron bandwagon. I think you know that.
Morley Robbins:But they need to start to recognize the critical biochemical, physiological role that goes back to the beginning of time for being able to harness iron and oxygen at the same time. Iron mass per pro-oxidant on the planet, oxygen, second most reactive element. And what do they like to do? They like to play together and what do they create? Rust.
Morley Robbins:And so people need to realize that the plaque and all the dysfunction inside their body is an expression of rust that we recognize outside the body.
Morley Robbins:Just, we never been told that that rusting process was happening inside our blood vessels and our nerves and our tissue, and so I think people need to the test that we do within the RCP community. It's called the Full Monty Iron Panel and there's panels available in Australia and in Europe and here in the States and people. There's about 13 different components to that test and we're looking at different measures of iron, we're looking at copper, we're looking at ceruloplasma, we're looking at urag acid Urag acid building in a body is a clinical sign of copper deficiency. We're looking at vitamin A and vitamin D and the relationship between the two and a variety of other factors, and people can begin to get a deeper understanding of their basic mechanics, mineral mechanics, from that blood test. And it's a very easy test to do and it's just. It gives the practitioner and the patient tremendous insight about the ease and efficiency of their energy producing ability inside their body.
Dr Max Gulhane:Yeah, fascinating, and we'll include that information for people who are interested in diving down. One last question for you, Molly Do you ever do? Have you ever looked into a peripheral blood smear? Because you know Dr Cruz said once that the kind of thing he's interested in is looking at the oxidation state of iron Like that in terms of examining a blood smear. Have you ever done that, and have you ever gleaned any kind of useful information about copper or iron status from that test?
Morley Robbins:No, I've never done the peripheral blood smear. I would love to delve into that. But what I do know is that a lot of people suffer from neuropathy in their peripheral tissue and I first connected with Dr Clavet, who I alluded to earlier. It was probably 10 years ago and it was very gracious to take my call and we've talked many times since then. But he said Moorley, if any of your clients ever present with any form of neuropathy he said it's a clinical sign of copper deficiency.
Morley Robbins:And when someone of that stature makes a statement like that, I take note and I've all helped. A lot of people realize that that nerve sensation that they were having is really just a dysfunction and a deficiency of the mineral. And so I don't know the components of a peripheral blood smear but I'll look into it and see what I can glean from that. But I'm pretty confident that iron is not being regulated properly in that blood smear. The oxidation state is probably not being regulated properly in that blood smear and it's going to go back to a series of copper enzymes and their dysfunction because they're not adequately energized. It would be my initial comment.
Dr Max Gulhane:Yeah, and I would add in B12 replacement. And if someone presents to me with peripheral neuropathy, I'd definitely be checking their serum B12, too, which is definitely a possible cause, additionally, of peripheral neuropathy. I think this has been a very good one.
Morley Robbins:Do you know that you've heard of the intrinsic factor? Yeah, yeah. What is the intrinsic factor called it's protein? It's a transport protein called cubulin. It's copper dependent it's copper dependent.
Dr Max Gulhane:There you go there you go.
Morley Robbins:No, I said that the symptoms of B12 deficiency and copper deficiency are almost identical, max, and so that's important for people to realize the vitamin B9 folate. One of my conversations with Dr Clavage years ago I said I have this theory that all the B vitamins require copper and they regulate iron. He said well, more or less, that's a very provocative theory so I can't refute it or defend it. He said but what I can tell you for a fact is that B9 is copper dependent. Well, when you think about what B9 does in the production of vitamin D, in the breakdown of vitamin A, your whole understanding of the mechanics of those fat-soluble vitamins changes in a flash because you realize, oh, b9, it's reacting to the sunlight. Oh, it must be the copper inside the B9 that is attracting the sunlight. It completely changes your understanding of the dynamics of the chemistry.
Dr Max Gulhane:Yeah, and that's another thing that Kruse has talked about is the non-visual photoreceptor function of vitamin B12. And, yeah, at the core of a lot of these visual properties is these minerals. So, yeah, it's a fascinating conversation that we've had. Molly, thank you very much and I'll include those If you can send me those. There's that information. I'll include that in the show notes. And there's a lot we haven't even talked about. We haven't talked about iron dysregulation as it relates to cardiovascular disease, and perhaps we could talk a bit more about metabolic syndrome in another time, and obviously, magnesium too. So lots for people to think about and yeah, so thank you very much for your time and I guess, yeah, we'll definitely have to talk again.
Morley Robbins:I look forward to it. I really appreciate the time and the exchange has been fascinating.
