Morley Robbins (Part 3) – Copper vs. Iron, Vitamin D, C, A, Zinc, and more

Content By: Ari Whitten & Morley Robbins

In this episode, I am speaking with Morley Robbins about his novel hypothesis that chronic fatigue (and most chronic disease) is caused predominantly by copper and iron dysregulation. This is a fascinating idea that I allow him to explore in depth, while also pushing back a bit at times on the idea that health can be reduced to any kind of simple mineral issue. In this part 3, Morley will tie the previous episodes together and share the next steps to improve your health.

Table of Contents

In this podcast, Morley and I discuss: 

  • Is ferritin really a good biomarker of health?
  • The pitfalls of consuming supplements
  • Blue light and how it affects our health
  • What high levels of uric acid indicate
  • And much, much more

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Ari: Welcome back, everyone, to The Energy Blueprint podcast with me. Again, for the third time in a relatively short period of time, is Morley Robbins, the author of this book, Cu-RE Your Fatigue. He has now been on the show two times recently, hopefully, you listen to those two prior podcasts. I have a hunch knowing Morley, that if you don’t listen to those two prior to this one, it might be hard to understand some of the material that we get into today, I’m guessing.

There’s a lot of background here, hence the reason that we’re doing three episodes is because there’s a lot of material here to unpack to fully understand more least paradigm of human health. We have some more exciting stuff to talk about today. We’re going to be talking about some relatively new insights that Morley has around uric acid. We’re going to be talking about iron deficiency anemia versus anemia of chronic inflammation, something we talked quite a bit about in part two, but I want to have him wrap that up and put a nice little bow on it.

Morley: [laughs] Christmas present.

Ari: I suspect our conversation might twist and turn into other avenues that we have not expected or planned. Morley, let’s get into it.

Morley: All right. It’s great to be here. Thank you for the opportunity and I’m looking forward to tying pretty bows on what we’re talking about.

Ari: Excellent. This is pretty unprecedented for me to do three podcasts with someone like this, so-

Morley: Wow. I appreciate that.

Ari: -you’re a very special person as far as The Energy Blueprint podcast is concerned.

Morley: No, I’m honored. I found that it takes a good two to three, sometimes four bites at the apple to get people to really, “Oh, okay. Now I’m beginning to–” The pieces of the puzzle are beginning to flow altogether. I think the challenge is that so much of what we do understand, but then don’t understand, stems from one phrase, missing information equals missing truth. The information that’s available on the internet, I don’t think it’s complete.

That’s just the life that we live now. That there’s a narrative that they want us to know. I’m not sure they want us to have mastery of the nature, the natural forces behind things. When it comes to energy and the blueprint for energy, you really need a much more complete understanding of what’s going on.

Chronic inflammation anemia versus iron deficiency anemia

Ari: Excellent. I’m excited to get into that. I forgot to mention in my list of topics we’re going to get into, the most important thing that I want to make sure to cover today is some practical aspects around your root cause protocol to actually help people resolve a lot of these core issues that you’ve been unpacking these past two and what will now be three episodes. Make sure everybody listening, to stay tuned because we are going to get into. This is not going to only be theory and talk of mechanisms, we’re going to get into some practical nitty-gritty stuff here as well. Morley, let’s start by putting that bow on chronic inflammation anemia versus iron deficiency anemia.

Morley: I think it’s really important for people to draw the distinction between low iron in the blood versus high iron in the tissue. We’ve been trained to believe that the blood is a perfect representation of what’s going on in the tissue, and it’s not. That’s the important work of Bruce Ames 2004, where there can be 10 times more iron in the tissue than what shows in the blood. We have a very skewed understanding because of the nature of the blood work.

What’s really important for people to understand is that there is an iron recycling system in our body. Every second of every day we’re replacing 2.5 million red blood cells. It’s a lot. Every second, 2.5 million, and in the course of the day, it’s 2 billion red blood cells that need to be replaced. It’s a lot of red blood cells over the course of a day. What’s surprising though is that in order to replace that, you only need 25 milligrams of iron. That was first identified by a preeminent hematologist named Max Wintrobe back in the ’40s, and he wrote a very important article to the Journal of Biological Chemistry. I think it was in ’42 or ’43 when he wrote the article, but he identified it as 24.4 milligrams of iron. He was very precise about it.

What is also important to know is, where is that 25 milligrams of iron coming from? We’ve been trained to think it’s coming from our diet, that we have to ingest 25 milligrams through our mouth. It’s a very important understanding, is the only way we can regulate iron levels in our body is through our mouth. We shouldn’t be ingesting it as much as we do. The only way to get rid of excess iron is through gravity, and it’s called a blood donation.

What’s important about the iron recycling system is that 24 of those 25 milligrams are coming from the recycling system. There are cells in our body called recycling macrophages, and those are the Pac men that gobble up the dying red blood cells. Principally in the spleen is where this is taking place. They’re turning over the iron that’s in the red blood cell. They have a back door and the back door of those macrophages and in many other cells, but in particular, the macrophage is called ferroportin iron doorway, ferroportin. It requires a copper doorman, and it’s a protein called [unintelligible 00:06:54] and it expresses an enzyme called ferroxidase.

What ferroxidase does is it changes Iron (II) into Iron (III) so that it can be attached to transferrin so that the iron can go back to the bone marrow where it gets made into the 2.5 million red blood cells a second. What’s important to understand is that when the ferroxidase enzyme is present at the iron doorway, the iron comes out two and a half times faster. That’s a big deal. Instead of going 20 miles an hour, we’re going 50 miles an hour. That’s a good thing. It’s important for people to realize that mother nature has this covered, but we do need 1 milligram of iron to add to the 24, and that does come through our mouth.

The challenge we’ve got in the modern era, ari, make sure I got that right. The challenge we’ve got is that we’re eating iron-fortified foods. We’ve got supplements that have lots of iron in them because there seems to be a downplay of the iron recycling system and a belief that we need every day to have a de novo intake of 25 milligrams of iron. I’ve seen some supplements, particularly prenatals, that go as high as 65 milligrams of iron, which is outrageous levels of iron.

People need to realize that our body does have a natural ability to recycle the iron. Whenever iron looks low in the blood work, low hemoglobin, low serum iron, low ferritin, what’s important for the practitioners to do is to rule out anemia of chronic inflammation, which is caused by a lack of bioavailable copper. I think the notion that everyone is iron-deficient, makes no sense on a planet where iron is the number one element. 30%, 36%, 34%, it’s a significant percentage of the earth’s composition is iron. It doesn’t pass the sniff test that the most evolved species can’t metabolize the number one element.

There’s more to the story and when you get into the literature what you’ll find is you can’t make heme without copper. You can’t make hemoglobin without copper. You can’t make red blood cells without copper. The confusion is, only 1% of copper is found in the blood, 46% is found in the bone marrow, another 26% is found in the muscle. 72% of our copper is found outside of the blood. The mistake the practitioners make is interpreting a mismatch between copper and ceruloplasmin thinking that the person is copper toxic, when in fact they’re inflamed and the body’s responding to an inflammatory process. One of the topics that I’m hoping we get into is one of the major sources of inflammation is uric acid. That’s a byproduct of changes that have been made in the food system. People need to understand that there is a real solid reason why inflammation is rising in humans. It’s a function of changes in the farming system and food processing system that are causing–

Ari: Morley, let me ask you this real quick. Let’s say you have low copper levels and you’ve got this chronic inflammation that you’re describing, let’s say it even shows up as anemia on the blood tests, would you expect to see– would you always see, maybe is a better way of phrasing it, elevated markers of systemic inflammation like CRP for example, or other markers or is it possible to have this chronic inflammation that you’re describing without any elevated levels of any particular inflammatory biomarker?

Morley: Right. It depends on the sophistication of the biomarkers. C-reactive protein, I think is a misnomer. It elevates when there’s an infection, it doesn’t elevate with inflammation. I would argue that the C and C-reactive protein is copper-reactive protein. When copper comes on down, that’s when that protein seems to trigger. Again, the body is not being malevolent by releasing copper. It knows that copper is antipathogenic.

All the pathogens, bacteria, fungus, virus, and parasites, all cave in the presence of copper. There’s a wisdom to the body’s immune system to say, “Man, we need more copper in the system to get rid of these pathogens.” That’s not properly taught, I don’t think in practitioner school. If you get into you might get, T-bars are going to go up because of increased lipid peroxidation, you’re probably going to get elevations of tumor necrosis factor alpha or Interleukin 1 alpha or Interleukin 6. Those are very likely going to be spiking in an inflammatory situation.

LPS might be going up, Lipopolysaccharides might be going up. I think not many practitioners are going to do that deep penetration of markers. I think you should find those markers are elevated in a copper-deficient state that appears to be some kind of disruption to the iron recycling system. Does that make sense?

Ari: It does, yes. Is there anything else that you want to say on this topic of anemia, of chronic inflammation?

Morley: Well, I think it’s– Go ahead.

The prevalence of iron deficiency anemia misdiagnosis

Ari: Maybe, let me ask this. What percentage of people who are currently being diagnosed with iron deficiency anemia as they get blood tests or standard physical exams, and tests comes back showing signs of anemia. Doctors saying, “This is a sign of iron deficiency, take some iron supplements, eat red meat.” What percentage of those cases do you think are actually this iron anemia of chronic inflammation?

Morley: 99%. I think the only condition of true anemia of iron deficiency, AID, is someone who’s been in a traumatic accident where there’s been significant blood loss. I think otherwise it’s a dysregulation between copper and iron in managing the recycling system. I think it’s the most over-identified diagnosis because of a fixation on iron and a total lack of awareness of the role that copper plays to regulate all facets of iron metabolism. These are not my theories. These are Douglas Kell and [unintelligible 00:14:54] Richard Howell, Robert Crichton, some of the really big iron biologists know how important copper is.

The narrative is, “Oh, we need more iron.” We need to get beyond that narrative because we know there’s more to the story. There’s a lot more to the story. That’s why I appreciate these conversations is you’re giving your listeners a chance to wake up and like, “Whoa, wait a minute. There’s more to this process.” Again, people get fatigued. They’ll be diagnosed with anemia. Anemia is actually low hemoglobin, technically that’s what hemoglobin or the anemia is really referring to the hemoglobin level.

They’ll have fatigue and then they’ll say, “Take more iron.” There is a spike in hemoglobin when you take any heavy metal, arsenic, lead, mercury, there will be a spike in red blood cells. It’s short-lived. Again, that’s the wisdom of the body trying to bring more oxygen to get rid of this heavy metal. People have been seduced into believing that this is the right thing to do, and I need to keep taking iron because I need a hit about every six weeks, maybe eight weeks in order to really keep my energy level.

Well, Robert Hodges in 1978 [unintelligible 00:16:29] that issue and it’s a very slippery slope to throw iron at a copper deficiency problem. There’s a calculus to iron or calculus to the role that copper plays and what has happened as practitioners are using iron rulers to try to solve a copper calculus problem. That’s the mistake that keeps being made.

Why iron is problematic for health

Ari: I want to talk a bit more about something that I think is central to everything about your paradigm. Central to your paradigm. Yet I feel like we haven’t quite explained it yet with clarity. That is the importance of blood levels of iron versus this stored body iron and what is this iron actually doing? Why is this iron so problematic? Can you describe that very succinctly?

Morley: Iron is meant to be in circulation. Iron is meant to be moving, iron is meant to be recycled. What’s happened as of 1972, Jacobs [unintelligible 00:17:47] in the British Journal of Medicine, BJM, do I have that right? They moved the spotlight away from hemoglobin to ferritin. Now, in the modern era, after 50 years since that publication, exactly 50 years, I think it was July of 1972, I remember stuff like that, I don’t know, but I do. The thing is stored iron is not your friend. We’ve been trained in the modern era to believe that it is. Iron is meant to be in circulation, meant to be moving, and in order to be moving, in order to be recycled, there must be bioavailable copper.

It turns out that there are four different forms of ferritin, I don’t know whether you know that or not, but there’s two forms of what are called heavy chain ferritin. Heavy chain means that you must have ferroxidase enzyme function to get the iron in, but more importantly to get the iron out. Those are ferritin heavy chain and mitoferrin, which is found in the mitochondria.

Then there is another form called ferritin light chain. Well, light chain doesn’t have the ferroxidase function, so it’s very good about accepting iron. It’s not very good about letting it go. Where people get really confused or deceived is that if the body cannot recycle that iron, it will denature the ferritin and it will become hemosiderin. Hemosiderin is not measured in a blood test. Have you ever done a hemosiderin blood test?

Ari: Nope.

Morley: No. That doesn’t surprise me at all. Hemosiderin holds 10 times more iron than ferritin. It’s a toxic waste dump for iron. It shows up in brown splotches on your body, especially below your knee. You know you’ve got hemosiderin if you start to see big freckles below your knee, people with diabetes very often have that or heart disease. The thing is, there’s a fourth form of ferritin and it’s called serum ferritin. What is serum ferritin? What’s supposed to happen is when that ferritin light chain and L for liver ferritin, heavy chain heart.

The liver likes to store iron. It’s good at it, especially when copper’s low. The book ends of the research on that are 1928 by Heart [unintelligible 00:20:53] and 2021, Kim and Gonzalez figured it out genetically that when copper’s low, iron’s going to rise in the liver, the ferritin light chain gene is going to go crazy. It’ll be more expression of the ferritin light chain protein and that the iron in that ferritin light chain needs to be broken down in the stomach of the hepatocytes, the lysosome.

When the body doesn’t have enough copper in the lysosome to create the high energy peptides to break down that protein, iron gets dumped in the liver, in the hepatocyte. Then ketamine or acids are cleaved off of the ferritin light chain. Then what gets secreted into the bloodstream is what’s called serum ferritin. It’s empty shotgun shells. In extreme inflammation in the liver, you’ll have high serum ferritin, and extreme situations in the spleen, you’ll have low ferritin and parasites are involved in this process.

The research around it is very subtle, but very significant. None of this, the distinctions of four different types of ferritin, the fact that two of them require bioavailable copper, the fact that the serum ferritin and that’s showing up in the blood, there’s no iron in it. That’s not me speaking. That’s Warwood, Lusio, Kell, these are really big names in iron biology. The intelligence, they just don’t teach it to doctors or to other practitioners. There’s a lot of misinformation as it relates to iron metabolism and technically it should never be called iron metabolism. It should be called copper-iron metabolism because copper’s the general and iron is the foot soldier. That’s an important distinction for people to recognize as it relates to who’s in charge and who’s calling the shots.

The healthy levels of ferritin

Ari: Okay. Now, in your book, you wrote something to the effect of the lower the ferritin levels, the better.

Morley: Right.

Ari: Within, obviously, conventional medicine as you’ve alluded to and as any quick Google search and article will say if you look up ferritin, it will give you a range and it will say, you can be too low. If you’re outside of this range above a certain value, that value differs a bit depending on which article you’re reading and which source you’re looking at.

They say if you’re below this level, that indicates iron deficiency anemia, which is something that you basically say doesn’t exist and you’re saying the lower the ferritin, the better. Is that correct? How can you be so sure that everyone has gotten this wrong? Meaning there seemed to be a variety of articles, studies online talking about ways of inducing iron deficiency by, for example, chelating iron out of the body and that this results in anemia. How is it that you’re that confident that basically the lower your body levels of iron, the better?

Morley: No, that’s great question. Again, I come at it from a standpoint of understanding that you got to look at the three containers of iron hemoglobin which is a bucket, serum ferritin, which is a teacup, and serum iron which is a thimble. You need to put it into the context of copper metabolism and vitamin A and D metabolism. I’ve worked with a lot of people and I see a very consistent pattern.

I was just talking with someone who has one gene defect for a ceruloplasmin anemia, which means she’s not making ceruloplasmin at the rate that she should. There was a period of time where she was taking iron supplements, high doses of vitamin D, mega doses of zinc. I was able to explain and connect the dots back to why her liver was overwhelmed by those nutrients to lower the production of ceruloplasmin.

She said, makes perfect sense. She says, “No one’s ever been able to explain that to me.” The thing is, I think what’s missing, Ari, is a deep enough understanding of the general copper and that iron serves at the pleasure of copper. That’s not the consciousness of practitioners. I’ve talked to hundreds of doctors, all of whom have told me that there was only one mention of ceruloplasmin in their four years of training and it related to Wilson’s disease. They could pass that test. That’s it.

That’s pathetic as far as I’m concerned. To me, it’s smacks of a bias in the training because when you get into the literature, you find out how elegant and significant copper is to regulate iron. The origin of– we have to be careful about the lower the ferritin, the better. The range that I use is 20 to 50. I like to see it closer to 20.When the flags pop up in a woman when it’s above 150 and when it’s above 300 in a man and when it gets below 20, everyone gets nervous and has convinced our iron deficient.

Well, many years ago, 2018 I had an opportunity to talk to Douglas Kell, world-renowned iron biologist, very applicable guy about my age, wall of books behind him. I asked him, I said, “What’s the ideal ferritin for a human being?” He said, ”Zero.” I about fell out of my chair. I said, ”Excuse me?” He said, ”Morley, I want to make sure you understand this. Rising ferritin in a blood test is not a sign of iron vitality. It is a sign of organ pathophysiology. Do you understand what I just said?” I said, ”Yes, sir, I do.”

What he was referring to was that recycling process with the lysosomes. What I’ve since learned is that there’s actually a really critical transport protein to bring ferritin into the lysosome so that it can be broken down. It’s called NCOA4. You’ll be delighted to know, Ari, that it’s a copper-dependent transporter. If copper’s not there, the transporter can’t get the ferritin where it needs to be to break it down.

It’s like, oh wow, that’s a serious problem. It leads to misinterpretation and misunderstanding about what is the true iron status, particularly as it relates to ferritin. Again, we got to come back to the fact that there’s four ferritins in the body, and let’s be really clear about that. To put all this emphasis on serum ferritin, which is a denatured form of ferritin that didn’t get properly recycled because the NCOA4 wasn’t working. Well, I think that’s really significant.

I think what I have is a broader understanding of true copper-iron metabolism. I’m very confident, I hope I don’t come across arrogant because that’s not my intent. It’s interesting. I just had the release of my third conversation with Dr. Joe Mercola and he was picking it at being on the same issue. He said, “So you’re telling me that everyone else is wrong and you’re right? I said, ”Pretty much.” I’m not trying to be obnoxious about it. I’m trying to wake people up. What I really appreciate is your willingness to stay with this dialogue to make sure that not only that you understand it, but that the folks who depend on you and follow you, and rely on your intellect, they begin to understand it as well because what we can agree on is that the training of practitioners is woefully incomplete.

I would argue that the biggest defect in clinical training is the absence of any discussion about the role that bioavailable copper plays for a whole series of regulatory enzymes that regulate nerve action, neuropeptides, iron recycling, energy production, digestion, you name it. That’s completely expunged from the training, which I think it’s an egregious error on the part of, how practitioners come out of their years and years of training.

Ari: You said a couple of things that I just want to clarify briefly. One is, you said, we have to be careful with this thing the lower the ferritin, the better. You recommend a certain range of 20 to 50, yet you spoke to this famous iron researcher Douglas Kell who said that the optimal level is zero. Why do you disagree with him?

Morley: It’s unbelievable. No one would believe me if I said, “Let’s go for zero.” I made a unilateral decision to bring it up to 20. I think it’s an acceptable range in an era where people are bonkers about iron.

Ari: In general, you do agree with the lower the better. I totally understand this, to some extent, probably to not make yourself vulnerable for being attacked by conventional authorities who are going to say this guy’s nuts. He’s recommending a ferritin level of zero.

Morley: Douglas Kell has doctorates. He’s a knighted scientist in England. He’s got certificates and an endowed chair. He can say zero. I don’t have that.

Ari: All right. In general, the lower the better. Now, having said that, very central to your approach should be lowering the body stores ferritin levels of iron, the body load of iron. Is that correct?

Morley: No. It’s the root cause protocol focuses on let’s increase bioavailable copper and let’s deal with the iron. Copper is going to know what to do with the iron but in most people’s situation, they have excess iron in their tissue that’s never been able to get out because the copper doorman was not there to release the iron into the recycling system.

Ari: Okay, got it. Ideally, you are interested, you do recommend lowering the body’s levels of iron through blood donations. It sounded like from your perspective, that’s the main way and now it also sounds like optimizing copper levels, and ceruloplasmin and these other copper-dependent enzymes allows for copper to be handled correctly in a way that makes it less toxic.

Morley: Exactly. Again, there is a wisdom to the body. I firmly believe that what the immune system relies on is energy and intelligence. That’s what the general brings to the process.

How curcumin affects copper and iron levels

Ari: There’s one compound that I found actually while I was reading up on this topic in preparation for more conversations with you, and I’m surprised to not hear you talk about it. I don’t believe it’s in your book or your root cause protocol, but it seems to have quite a number of studies showing that ferritin levels lowers the body’s level load of iron in the tissues by chelating iron. Do you know what I’m compound I’m referring to? It’s a natural compound.

Morley: It might be curcisin but I’m not sure.

Ari: Curcumin.

Morley: Curcumin. Okay, sure.

Ari: Curcumin, there’s a number of studies and most of these are framed in a negative way. For example, here’s curcumin may impair iron status when fed to mice for six months, so they’re talking about like worried that it would lower iron levels too much. Here’s a case study talking about iron deficiency anemia due to high-dose turmeric. This one is describing somebody, a 66-year-old physician treated himself for osteoarthritis with six turmeric extract capsules daily to help with inflammation. During this time, his hemoglobin never rose above 12 and his iron and ferritin levels were consistent with iron deficiency.

Here’s another one just for the sake of mentioning that to show that the mechanisms have been studied, and this clearly does lower iron levels in the body by chelating it is this one’s in the journal PLOS One and it says curcumin attenuates iron accumulation and oxidative stress in the liver and spleen of chronic iron overloaded rats.

Morley: I’ve got a product called recuperate and there’s turmeric in it.

Ari: Interesting.

Morley: The thing is, you have to be really careful about the sourcing of that herb, or that spice. I guess it’s the spice because what you’ll find when you have your quieter moments, Google curcumin, copper chelation, and you’ll find that it chelates both copper and iron.

Ari: I actually found one of these studies I’m trying to remember which one, I don’t want to go digging for real-time here, but I’m pretty sure one of the studies I read– I think I found it here. This is the one titled, “Curcumin may impair iron status when fed to mice for six months.” They specifically say right at the top and the highlights, “Curcumin chelated iron, but not zinc and copper in vivo.”

Morley: There are studies where it does do that. Again, we’re back to the quality of the spice, the conditions of the test. Again, where’s curcumin used extensively? In India.

Ari: In India.

Morley: Where is there a lot of iron in the planet? India. What’s the diabetes capital of the world? India. The thing is, the historical Indian diet is not offsetting the iron crisis that their ancestors were able to manage through their diet. There’s been changes in the food system, I would argue and then the pharmaceutical system that are working against the natural impact that curcumin has had generationally. Again, there’s too many variations, that I don’t really rely on that as a source of iron chelation.

Ari: A very brief, high-level, 30,000-foot view quick summary of what we’ve talked about in these podcasts thus far and this is going to miss a lot, but I just want to focus on just this piece of it. Copper is central to human health. There’s many, many different mechanisms, enzymes, pathways, proteins, antioxidants, redox status of cells, inflammatory pathways, oxidative stress pathways that critically depend on optimal levels of copper and ceruloplasmin in the body.

Iron overload is a huge problem. Most people are accumulating too much iron and this is exacerbated by the fact that most people are simultaneously copper deficient, and thus can’t handle the iron appropriately. As a third layer going back to podcast number one, there are many different factors in the modern environment and lifestyle that are lowering copper levels further, whether we’re talking about glyphosate, other toxins, or other factors that are excessively limiting copper levels in the body. Is that a fair quick summary of those two points around copper and iron?

Morley: Right. The only thing I would add to that is that if copper is not at optimal levels of bioavailability, the oxygen can’t be activated and turned into water to release the energy molecules. If it can’t be activated, it’s going to be turned into oxidants. It’s the reactive oxygen species that begin to trigger the immune system that begins to trigger the symptoms that people are responding to.

Uric acid and blood sugar

Ari: Got it. Having said that, all of that about copper and iron, I think now is a good time for us to move to uric acid. How does uric acid fit into this story? I don’t know to what extent it fits into the story or its own story. Tell me about your insights into uric acid and why you feel it’s a critical player in metabolic health.

Morley: I think it’s a huge unknown. I think more people are becoming aware of it. There’s a famous article written in 1981 by Bruce Ames talking about the antioxidant properties of uric acid. Now 40 years later, uric acid is the source of metabolic syndrome. Wait a minute. It can’t do both. It can’t be a master antioxidant and a master prooxidant. What’s going on?

Again, I’m reading lots of articles. I’ve got a couple of books that I mentioned, one by Dr. Johnson, another by Dr. Perlmutter. This morning it finally just like, it clicked. I was like, “Oh man, I really want to be able to nail this with Ari.” What’s important to know is that there’s been a tenfold increase in our exposure to fructose. During the period of 1970 to 1990, high fructose corn syrup changed everything.

What was also playing in the background, 1970 to 1990, farming used glyphosate. You have this double whammy effect of what a lot of people may not know is that in order to metabolize fructose in the liver, you got to use something called the polyol pathway. The polyol pathway chelates copper, takes it out of the system in order to break down the purines and the ATP to ADP to AMP to hypoxanthine, xanthine, and then finally uric acid. You’re pulling copper out of the system.

Ari: That’s to break down and metabolize fructose.

Morley: Yes. I think is a really important contribution by Richard Johnson. He highlights the fact that the biggest sources of fructose are high fructose corn syrup, fruit sugars, of course, alcohol, a high purine diet, and the one that I’d never seen anyone identifying, which I think is really, really important, stress. When we’re under chronic stress, the body is going to convert our sugars into fructose. I don’t fully understand why it does that, but that’s the adaptive process of our metabolism under chronic stress. What–

Ari: Hold on one second. It’s converting which sugars into fructose, that the glucose that’s floating around in our bloodstream, glycogen stored in our body?

Morley: Yes.

Ari: It’s converting it into free fructose floating around in our bloodstream?

Morley: Absolutely.

Ari: I’ve never heard that.

Morley: I know. Again, this is not Morley speaking, it’s a very important book to read.

Ari: Richard– For people listening, Morley’s holding up on the video screen, the book by Richard Johnson, Nature Wants Us to Be Fat, which I have not read, I can’t comment on.

Morley: It’s an amazing book. I’m only halfway through it. He has compelling evidence that under stress, there is this uptick in endogenous production of fructose. It’s like a wow. What he is talking about is that he claims that switch and that under stress, the body defaults to making fat. He says nature wants us to be fat. I don’t think that’s true. Nature wants us to be in hemostasis.

The rephrasing of his comment is we default to triglycerides when we are under chronic stress. Now, what people need to understand is what does chronic stress mean? When you have a lack of bioavailable copper and you can’t deal with that oxygen, that is chronic stress, that oxidative stress that’s produced in that state begins to work against our metabolism.

What’s important about this is as you get into the subject matter of uric acid, what you find out is it’s like a wet blanket over the mitochondria. You talk about the blueprint for energy, energy blueprint. If you want to kill energy production, increase the level of uric acid in the cell, and very effective, it’ll zap it.

What I’ve come to realize is, again, we have this dietary source of fructose versus the stress-induced source. That’s an important distinction. We have acute synthesis versus chronic synthesis or acute exposure to fructose versus chronic exposure. Then we have that, there’s a whole dynamic about are we making it or are we clearing it fast enough? We’ve got the dynamic between the liver and the kidney. Dr. Johnson is a nephrologist, so he is been studying this for a long time in his career.

Dr. Perlmutter of the other book I’m reading is a neurologist, but uric acid is really critical for both kidneys and the brain in terms of being a good guy and a bad guy? The thing is, it turns out that there’s a lot of confusion. Again, back to my comment about Dr. Ames, is uric acid an antioxidant or is it approximate? It really has to do with the uric acid in our plasma that being the liquid that carries the red blood cell, is the uric acid there, or is the uric acid building inside the cell as a result of xanthine oxidase breaking down hypoxanthine to xanthine to uric acid. What’s given off in that process is an oxidant called superoxide.

When xanthine oxidase becomes problematic, it’s because there’s a lack of superoxide dismutase, which is a copper-dependent enzyme to clear superoxide. The real crisis isn’t just our exposure to fructose, is, is there proper levels of copper in our body, in our tissue, in our cells, to deal with the oxidative stress that comes from this uptick in the breakdown of fructose?

Everything clicked this morning when I learned there are– I knew about these metabolic pathways, which I’m sure you know about, mTOR versus AMPK. What’s important for people to understand is that mTOR is Cain and AMPK is Abel right out of the Bible. What did Cain do? He killed his brother Abel.

An mTOR is really good. mTOR is really good at killing AMPK. What AMPK is really designed to do is increase that metabolism. What activates mTOR? Iron. Iron is the fastest activator of mTOR. Very powerful. What’s the connection with AMPK? It kills off copper, but what’s important is that in order to have proper fat metabolism, a very critical enzyme called PDE2, phosphodiesterase 2, needs to have a copper atom present so that phosphodiesterase 2 doesn’t do its job so that proper fat metabolism can take place inside the cell.

What happens is if copper is not optimal in the cell, what you’re going to have, particularly in the presence of increasing levels of uric acid, is you’re going to have an explosion in triglycerides. When triglycerides rise, suddenly the whole chemistry of the cell changes, and then the oxidative stress begins to take off like a rocket. It’s uric acid in the blood, that’s our friend. Rising uric acid in our cell, not so much.

There are many scientists who’ve been studying this dynamic. Ming Song at University of Louisville Medical Center in Kentucky 2012, 2015, 2018 did a masterful job of explaining how problems with uric acid are a result of lack of copper. Leslie Klevay has commented on this. [unintelligible 00:50:38] a French researcher also commented on this in 1993, but probably the most definitive author is Myra Fields. She was at the USDA and in 1996, she did a very important study to prove that it’s copper deficiency, it’s creating the crisis with the increased uric acid inside the cell.

Again, I know we’re getting into some very subtle metabolism and subject matter that maybe most of your listeners aren’t aware of but the reason why I’m so focused on it, Ari, is that this uric acid building in the cell is causing 40% of earthlings to have metabolic syndrome. 40% of the Earth’s population is facing some form of metabolic syndrome and it’s a crisis. It’s a true pandemic and people are not aware of it. They need to realize that it’s in part their fascination and fixation on fruit. Our ancestors never had the exposure of fruit that we have. The explosion of high fructose corn syrup, the explosion of chronic stress in our world, and the decimation of bioavailable copper.

In large part, because it’s not in the diet, but we don’t have enough retinol to allow for the proper loading of copper in its enzymes. We’ve got this, this very significant juxtaposition of nutrients. It’s leading us into this metabolic crisis called metabolic syndrome. I think it’s important for people to know that uric acid is in fact, the cause of insulin resistance, is in fact, the cause of hypertension, is in fact, the cause of cardiovascular disease, is in fact, now being labeled as one of the causes of cancer. Certainly, the biggest connection is with non-alcoholic fatty liver disease.

It isn’t just, well, this uric acid thing is confusing. It’s like this uric acid thing, it’s a double agent in the blood seems to be okay. When it gets in the cell, when starts to build in the cell because it’s being overproduced because of the lack of copper. Well, that’s when we have the crises that we’re now facing worldwide. Hopefully, that makes sense.

Is supplementing vitamins healthy?

Ari: Very interesting stuff, Morley. I want to transition now into the practical aspects of your root cause protocol. Let me start with just a few interesting points of philosophy. Key principles from your approach to healing. You say number one, the RCP, root cause protocol works from a perspective of health rather than disease, and the primary culprit of disease generation or the starting point of it is considered to be oxidative stress stemming from disruptions in mitochondrial energy production. Now we know a big focus of your work in that regard has to do with copper and iron and now uric acid is another layer to it.

The RCP favor strengthening the host as opposed to attacking the guest in regard to pathogens and toxins. I totally agree with you on that, by the way. Number three, while mainstream practitioners seek to flood the body with isolated synthetic versions of nutrients that are low on their blood testing, the RCP looks to why those nutrients are low and focuses on supplying the building blocks required to balance all elements naturally.

I also think is wonderful and number four is as much as possible the RCP recommends nutrients come from fresh organic food, rather than synthetic nutrients which lack the enzymes and cofactors that occurred naturally in whole foods to aid in their digestion, assimilation, and activation in the body. Also, wonderful. With that context, there’s a few things that you recommend not doing that are commonly recommended. Just for the sake of time, Morley, I know, you could probably give 20-minute-long answers on every one of these, but I want to try to get through as much of this as possible.

We’ll try to just get through in more like list form. If you could give me a succinct of answers as possible. I think that would benefit all of our time, just as far as getting through as much of these questions as possible. You recommend to stop taking iron supplements, that one’s very straightforward given everything you’ve discussed. You recommend to stop taking vitamin D3, calcium, and zinc supplements. Let’s maybe address those three briefly.

Morley: Again, they are contraindicated because they have massive impacts on the nutrients that we’re focusing on. Calcium blocks magnesium absorption, zinc blocks copper, but it goes on to kill the ferroxidase function of ceruloplasmin. I think it’s important for people know that. Again, and probably there was a lot of work done at the University of Michigan by George Brewer in the late ’70s, through the early ’90s, where he basically proved that, I mean, it’s like, why don’t more people know that?

The thing with Vitamin D, there’s probably no subject that I’ve been speaking out against, for as long than Vitamin D. In large part because it blocks the uptake of vitamin A. See, we live in an era now– Back in the early ’20s, retinol was the nutrient. It was like, “Oh my gosh, this thing is amazing. It’s a powerhouse.” What were they doing with vitamin D back in the 1920s? Throwing it away. Now we’ve become reoriented, and we know better. People don’t realize that A and D are Frick and Frack but when you start to hyper supplement with D, you’re going to block the absorption of A.

Well, when you block the absorption of A, it has many downstream impacts. What most people don’t seem to understand is it is not storage D that matters. Storage D is parked cars. What you want to focus on is active D. Those are cars on the autobahn. When you’re on the autobahn, you need a driver, that’s called VDR, vitamin D receptor. You need a driver, and you need a navigator and that’s called RXR. Active D, VDR, and RXR are a triad that must work together in order to stimulate the immune system. No one talks about that, or not enough people talk about that. Everyone is preoccupied with their storage D level and storage D fluctuates with the sun, with the seasons.

Why is storage D higher in the summer and lower in the winter? Because storage D is sunglasses. When there’s too much sunlight, storage D rises to block the light coming into the tissue. When the sun is beginning to disappear as it is now in the winter months, we’re coming up on the shortest day of the year and about 23 or 4 days. When that happens, storage D drops and it allows more lighting. Now what’s happened in the modern era, the Uber modern, the post-COVID era is we’ve been trained to believe that Vitamin D is going to pump up your immune system and you’re safe. I don’t believe that. Most of that research, the vast majority of that research is based on correlation, not on causation.

Ari: What explains the correlation? If not, its direct role in [crosstalk]

Morley: Again, the problem is that the illness is usually attached to Vitamin D, storage D deficiency and the illusion is let’s increase the vitamin D to offset what’s the perceived inflammation causing a low Vitamin D. What’s really causing low storage D is a lack of magnesium because the enzyme to make storage D is magnesium-dependent. Why is magnesium down? Because iron is building in the liver. Why is iron building in the liver? Because by available coppers not being made in the liver. There’s many moving parts, and they’re using this arbitrary marker and correlating it with conditions.

I think the work of Muhammad Amer at Hopkins in 2014 probably did the best job of neutralizing that whole issue. That he looked at storage D status versus all-cause mortality, and he found no benefit above 21 nanograms per deciliter. The world has been mesmerized in the modern era to believe that if I get more D, I’ll be safe. When in fact we got to go deeper than that. We need to understand what retinol is doing. We need to understand what the copper-loading enzymes are doing. ATP7A, ATP7B, all the copper regulatory enzymes, energy production, and this simplistic, I just need more D and I’ll be safe. The client I was just talking to, her storage D was in the 90s and she was a hot mess.

Ari: She was taking high-dose vitamin D supplements.

Morley: 5000 IUs a day and had been for several years. People have become deceived begins with D with the disillusion and the disinformation D and D that it, again, people don’t understand the depth of how our physiology really works and how interdependent A and D are with each other. I think it’s what I recommend, you’re very clear, I do recommend don’t take vitamin D supplements. They’re synthetic, they’re not doing what you think they’re doing. What I do recommend is you take cod liver oil because it has A and D in proper ratios, 10 times more A than D. I would argue that retinol is probably a hundred times more important than D when it comes to running your metabolism.

Again, I’m not a stranger to being controversial or being alone in my recommendations or my stance, but it’s just based on my research, I tend to gravitate to positions that are in stark contrast to the popular recommendations. Because I’ve learned over the years and over the decades is that conventional wisdom is garbage.

Ari: I’m tempted to go into a bit of a broader thing here. Maybe we can, I’ll do it and hopefully, we can do it briefly. I will say I’m wired very much the same way that you are in that regard as a sort of a contrarian by nature and somebody who questions authority. However, I think that it’s clear to me now that there’s pathology on both ends of this spectrum in the sense that there’s a very obvious pathology.

Especially, that has been made very clear over the last two and a half years of watching COVID unfold around the world of a large portion of the population that just believes whatever their governments and media tell them without any capacity for critical thinking or analysis, even when there is lots of evidence and common sense that should very obviously persuade them to do a bit more thinking and questioning of authority. A large portion of people seem to be incapable of it. They’re just built to follow whatever the orders are from whatever perceived authority is without any capacity for questioning that.

Clearly, a very concerning pathology and unharmful pathology as we’ve witnessed when something like this unfolds over the last two and a half years. On the other end of the spectrum, you have another kind of pathology, which is a certain kind of people who are wired to perceive everything that any authority figure tells them as almost default a lie. Everything is some sort of deception and lie and people are out to deceive.

I think that is clearly obviously wrong and there are many authorities who are doing good honest work and who are putting out good information that is honest and truthful and accurate and helpful, and it is anti-helpful for people to question that, to be locked into a mentality of, always doubting and being cynical and skeptical of whatever an authority figure says and assuming it’s a lie because it’s an authority.

Anyway, that’s personally how I like to think of things. Then the landscape in the middle is tricky. The modern world is very, very difficult to do good sense-making to accurately analyze evidence from many different perspectives. We have to account for political agendas that are presenting cherry-picked and not even to figure in overt misinformation, which is certainly a big thing, but presenting distorted narratives by selectively presenting information. This is a huge thing and has blown my mind to witness how much of the media just overtly censored and never reported on any of the evidence which countered any of their claims.

It’s just full-blown propaganda at that point when you are just ignoring mountains of evidence that contradict your claims. If somebody’s only getting their information from a source like that, they perceive that as truth and they have no idea that there’s all this evidence that contradicts what they think is true. Anyway, again it’s very difficult to do good sense-making, but we have to engage in this rigorous process of trying to evaluate all this different sources of information, different perspectives, accounting for different biases and cherry-picked narratives.

Then critically analyzing, hopefully, primary evidence of some kind and comparing it with our own body of knowledge and forming some kind of conclusion, which may be a weak conclusion if you don’t have a strong, a lot of expertise in that area or a relatively confident conclusion if you have lots of expertise in that area. The process is difficult and suffice it to say, but I’m just curious if you have any thoughts on that landscape and given that you are a contrarian by nature and that you’re wired to sort of be skeptical of what authorities are claiming, have you questioned the potential downsides of being wired that way?

Morley: No, I’m very aware that there’s risk in the polls, obviously the polarity of that model that you presented. Again, I come back to some of our opening comments a few minutes ago about what’s the focus of the RCP. It’s to make energy that, that’s the preem, it’s again, ignore the enemies, ignite the energy. I put everything in an energy paradigm. I said, well, what role does vitamin D play in making energy zero? What role does retinol play in making energy?

Oh my gosh, how much time have you got? Did you know that there’s a very important study by Hammerling 2016 where he talks about the role that retinol plays between complex III and complex IV inside the mitochondria? You’re a student of the mitochondria, you know that. It turns out it’s a four-part complex called the signal zone, and that the electrons from complex III ride down the tail of the retinol lipid to go to complex IV. It’s a big deal, and he’s the guy that figured it out.

Retinol is absolutely intimately involved in energy production. Retinol is intimately involved in stopping inflammation. Retinol is intimately involved in making bioavailable copper and making sure that the copper gets loaded in its regulatory enzymes. It goes on and on and on. I recognize that I am at times like an island in a sea of people who are challenging me. I’ll have another podcast later today where I know this is going to be the focal point of the conversation. I have enough research on my side.

I think what really galvanized my position, Ari, was when I learned about of the research, a Montrose T. Burrows, physician from Hopkins, graduated in 1909. In 1925 and in four articles in 1926, he was able to prove that lack of retinol causes cancer, it creates a Warburg Effect. What are we going to witness in the post-COVID era? We’re witnessing an explosion of cancer.

Ari: Because of retinol deficiency.

Morley: Yes.

Ari: Where is the retinol deficiency coming from?

Morley: The whole nature of what COVID has done is there’s been an absolute preoccupation with vitamin D. The COVID cocktail, ascorbic acid, vitamin D, and zinc kills by available copper and vitamin D blocks retinol uptake. I renamed COVID, coppers vanished, ID, irons dysregulated. I can assure you that everything’s going on in this era now relates to the mismatch of those two metals. The thing is, I worry about, in the same breath, that I’m mindful that I can be exposed because of my stance. I worry about the C of scientists and clinicians that don’t know, simply do not know that A and D are Frick and Frack and need to be studied together.

That copper and iron are general and foot soldier and need to be studied together. It’s important to realize that we’ve been given, again, missing information equals missing truth. We’ve been told what the truth is has been shoved down our throat, but we haven’t been given the full story. That’s what my research is designed to do, is broaden our understanding so we have a more balanced viewpoint of what’s really going on.

Ari: Let’s get back to a few more things here before we have to wrap up. Well actually to wrap up vitamin D, so what do you consider an optimal level of Vitamin D and how do you feel about sun exposure?

Morley: Sun exposure is amazing. It’s very, very important. Because it’s going to sulfate the D which is really key is Stephanie Seneff points out. I don’t worry about it. It does not need to be above 21. That’s the genius of Muhammad Amer at Hopkins. These ideas that it’s got to get up to 100, people don’t realize what that does to alter retinol physiology, which is then going to alter copper physiology, which is going to alter iron physiology, which is going to create symptoms out the union.

Ari: One more quick digression. I would be remiss if I didn’t ask you this. I know that there are some people who are critical of your work, some people who seem to be making a career out of being critical of your work, and one of whom I personally know to some extent, that’s been many years since I communicated with him. Who I know I think is on board with the whole low vitamin A. Vitamin A is it retinol, is it toxin? Just shows how confusing this whole thing can be for so many people. Because here we have you going on and on about all the benefits of retinol.

Of course, you’re actually more sided with conventional nutrition authorities in this regard who view vitamin A as a critically important nutrient vitamin. Yet there is this other position of vitamin A as a toxin, we should be lowering our vitamin A levels. I’m just curious if you have any thoughts on that paradigm as well, and the people who are critical of your work in that regard.

Morley: Right. Very aware of it. The issue is synthetic A versus retinol. They’re very different. Beta-carotene is not retinol. The retinyl palmitate is not retinol very different components. The other is not realizing how important copper is to retinol metabolism. We live in a very copper-deficient world, and a lot of people don’t have the bioavailable copper that they need in order to work with the retinol. Then I think the third, and this, I really learned this from a client in Germany who was told by this person that you’re talking about that he was a retinol toxic, his iron level in his liver was out of control and that was the problem.

It was iron toxicity that was being labeled retinol toxicity. I was able to prove it in his blood work. I think there’s there’s, again, incomplete information, incomplete understanding. There’s a popular narrative that, again, as soon as people say that copper is toxic and retinol is toxic, I know right away they don’t understand physiology of the human being.

Ari: A few more of these stops things that you want people to stop here. Multivitamins and synthetic B vitamins, why?

Morley: Multivitamins are all synthetic. The ratios, they’ve got too much calcium to the amount of magnesium, outrageous levels of iron to the amount of copper, outrageous levels of zinc to the copper. The B vitamins are all synthetic. People don’t know what the source of B vitamins is. The processing of B vitamins, it’s from coal tar derivatives. People don’t know what that means, but there’s 10,000 elements in coal tar derivatives. It has a very close relationship with iron, I would point out, but they only have names for 5,000 of the 10,000 elements. Now I’ve scratched my head and say, Well, how do they know there’s 5,000 others if they don’t have names for them?” but they do.

Ari: What elements are you referring to chemical elements, because my understanding is that there’s the periodic table which has, what is it, 79 or something like that elements?

Morley: It might be a little higher, but that’s good.

Ari: Or 179. That’s been many years since I looked at that.

Morley: I think it’s over 100, but that’s all right.

Ari: No, it’s like 101. That’s right. You’re right. What are you referring to as far, it’s 103. What are you referring to as far as these hundreds of elements?

Morley: Thousands, thousands.

Ari: Thousands of elements.

Morley: Again, I don’t have mastery of that research. I just know that in the articles that I’ve read, they refer to the fact that there’s a lot of toxic elements in coal tar derivatives.

Ari: They’re using the word elements, not literally in that regard. They’re more toxic molecules.

Morley: Exactly. Better said. You’re right. I think I firmly believe that B vitamins that are made by mother nature are really activated by copper. Their job is to help regulate iron. We’re back to the general and the foot soldier. The most notable B vitamin that I know for a fact is copper-dependent. In my conversation with Leslie with a, probably eight years ago I posed my theory and he said, wasn’t, he said, “Morley that’s a very intriguing theory.” He said, “I can’t speak for all of the B vitamins,” he said, “But what I can tell you for a fact is that folate B9 is copper-dependent.” When you look at B9 folate metabolism and you drop copper element to it, everything changes.

All of the confusion about folate deficiency is really copper deficiency. 1934, they gave three physicians a Nobel Prize for curing anemia and pernicious B12 anemia. They used the same product. Minot, Murphy and Whipple, two from Hopkins, one from Harvard. What was the product, B flavor? Well, when you look at the symptoms of B12 deficiency and then look at the symptoms of copper deficiency, the lists are almost identical. Oh, there’s this famous intrinsic factor when we talk about B12, right? We can’t live without that intrinsic factor. Do you know what it is? It’s actually called cubulin, C-U-B-U-L-I-N.

Anytime I see the letter CU, I begin to suspect, maybe there’s a relationship with copper. That would be my theory about cubulin being the intrinsic factor that they can’t identify as copper. Now they’ve tried to convince us that it’s cobalt or it’s cobalamin. I don’t buy that. I just don’t buy that, Ari. I know I sound like a heretic when I say that, but it’s like there’s a certain elegance and simplicity to human metabolism. When you’ve got these elements, B12 deficiency and copper deficiency appearing identically, then something is awry. I don’t have mastery of it. That’s why we rely so much on the desiccated B flavor. That’s why my recuperate has B flavor in it because of the nutrients in B flavor, which are amazing. 

Ari: A few more questions here. Synthetic ascorbic acid, synthetic vitamin C, another one of the common things people are taking right now in the COVID era. So many people have been recommending, “Take high dose of vitamin C, take high dose of vitamin D, take high dose zinc.” You’re saying all of these things are harmful to copper and ceruloplasmin. What is it about ascorbic acid that’s problematic?

Morley: In the original article in 1948 when Holmberg and Laurell were introducing the scientific community to ceruloplasmin, they very clearly stated that ascorbic acid denatures ceruloplasmin and causes the copper to leak out. There have been many other authors who’ve reaffirmed that. We live in a world where we are led to believe that ascorbic acid, which is the antioxidant shell of a six-part mechanism– vitamin C complex is an antioxidant. Ascorbic acid is a prooxidant shell.

Unfortunately, we don’t have the time given the window that we’re in right now to really get into the nuts and bolts of it, but it’s very complicated, it’s very involved. Tremendous controversy around this. There are people who feel that I am absolutely insane to take the stance that I do, and that’s fine, but again, I rely on the fact that someone like Earl Frieden, who was the Dean of Metal Biology at Florida State University from the ’60s to the ’90s, he was the man, and he wrote a very important article in 1968 in Scientific American. He referred to the importance of tyrosinase enzyme.

Well, tyrosinase enzyme, again, it has parallel functions with ceruloplasmin. That’s how important it is, what’s found at the center of the whole food vitamin C complex that nobody knows about. There are just certain subject areas where there’s innuendo and uncertainty and incomplete information. I take the stance that tyrosinase is profoundly important. What I think is intriguing is the prevalence of use of tyrosinase inhibitors in the food processing industry. I find that fascinating. Why would the food industry be so concerned about shelf life when in fact it’s going to affect our life? These tyrosinase inhibitors don’t just affect the food, they’re going to affect the individual eating the food.

All of the colors, just so you understand this, all of the colors from yellow to black are a function of melanin, which gets its energy from tyrosinase. When you get into the real subtle and sophisticated physiology of the human body, you find out that colors are everything. There’s a reason why ceruloplasmin, the locus coeruleus, and other key copper centers are sky blue because of the energetic function that they bring. It requires that blue color means that they can absorb red light, but they emit blue light. It’s a big deal.

When you get into the physiology of the body, yellow, blue, green, red, and purple are the colors that run our body. Again, yellow to black requires tyrosinase, and it’s a profoundly important enzyme that very few people know about.

Ari: A couple more here. Omega-6s, and are you only concerned about the so-called vegetable oil, soybean oil, corn oil, canola, these sorts of things, or are you also concerned with whole food omega-6s?

Morley: That’s a really important question. I’m most concerned about the heart-healthy oils, the processed oils.

Ari: I assume you’re using heart-healthy sarcastically there if you say.

Morley: Yes. I should have put quotes around that [unintelligible 01:24:53]. A lot of deception around that. Again, I don’t think we can get away from all omega-6. I don’t think that’s healthy, but again, in the same vein that we’ve been exposed to a tenfold increase in high fructose corn syrup in a 20-year period, I don’t know what the number is now in 2020 or 2022, no one talks about that. I think it’s actually gone up. The significance is omega-6, according to the research that Joe Mercola has done, omega-6 it’s like a rocket and continues to rise. That’s a very alarming trend in our environment that has massive implications.

As I learned from him in our last conversation, omega-6 is very much involved in uric acid activation. It’s like, “Okay, all these things begin to tie together.” High fructose corn syrup, omega-6 oils, iron fortification, and when we have this explosion of uric acid inside the cell that zaps our mitochondria, which then is going to invite all sorts of dysregulation. That’s what I think people need to understand is that it’s not 100 factors, it may only be a handful, at most a dozen factors that we need to control. That’s really what the basis of the Root Cause Protocol is to identify a finite number of, “Stop doing this and start doing these.”

Ari: What about carbs? Is there a relationship of carbohydrates we’re consuming in the diet and is it about carbs specifically or about glyphosate on refined and processed grains? Because one of your stops is, “Stop eating high-carb, processed, refined foods.”

Morley: Right. I think the issue is the glycemic impact that it has. The low glycemic carbs I think are fine. I guess it would be the less refined the carb, the better, and ones that would be more naturally found in a garden, whether it’s in the dirt or on a plant. I think the real issue is limiting the amount of sugar we’re exposed to in the course of our daily diet and in the course of our lifetime. I’ve got a whole presentation I do around sugar being white iron. People don’t realize the connection between sugar and iron versus the interdependence between fat and copper. Trust me, when you want to make energy, you want to be burning fat, not burning sugar.

There’s a big difference in energy production between the two. I think we’ve been corralled into thinking that, “Well, glucose is where it’s at,” and now this is our diet, well, our peers’ diet. I don’t think it’s you and me, but our peers’ diet has 150 times more sugar in it than our ancestors who lived in the late 1700s. 150 times more sugar is a lot of sugar and it has an impact in our physiology. It has an impact in our mitochondria. If we don’t have the nutrients to support that, then we’re going to have a problem.

We know we have a problem because diabetes is on the rise, insulin resistance is on the rise, metabolic syndrome is on the rise, so we are dealing with environmental changes in our food that have had massive impacts on our metabolism, and we just need to wake up to that reality.

How blue light affects health

Ari: The last stop I want to ask you about here is blue light. This is something I’ve talked a lot about over the years lot. I’ve talked a lot about circadian rhythm. You mentioned EMFs from electronic devices. What is it about or how does blue light and how do blue light and EMFs tie into this paradigm that you’ve presented?

Morley: Well, blue light is the opposite of red light. Red light is the frequency of copper, blue light is the frequency of iron. Blue light really messes up the suprachiasmatic nucleus, which really messes up our clocks. What’s important to know is that there are a bunch of clock genes in our body. Guess who the battery is in all those clock genes? It’s copper. Ding, ding, ding. That’s in the literature. When we’re exposed to, again, it’s all orders of magnitude, a little bit of blue light, not a problem. Technically, you and I should be wearing blue blockers because we’re exposing ourselves to this screen. Maybe you have blue-blocker contacts. I don’t.

Ari: Well, I don’t. I actually have blue-blocking technology built into my screen, but I’m not using it right now. I’m looking at a blue sky, which is lots of blue light entering my eyes. I just surfed this morning and had lots and lots of sunlight that contains lots of blue light entering my eyes. I can’t say that I agree with you as far as blue light messing up our suprachiasmatic nucleus. My understanding is blue light is essential for the suprachiasmatic nucleus in the circadian clock to tell day from night.

Morley: Absolutely true, but it’s the magnitude of exposure. Blue light is really cool when the sun’s up.

Ari: Yes. Exactly.

Morley: Blue light is very dangerous when the sun’s down.

Ari: That I agree with.

Morley: Right. That’s what we’re really referring to. It’s important for people to know that the environment that we live in now, it’s almost impossible to find incandescent light now. Everything, halogens, LEDs, all of these bulbs now are blue light. Really? That’s fascinating because an incandescent is full spectrum light, fireplace, full-spectrum light, but what we’re exposed to now is all blue light. Really? That doesn’t sound healthy to me. That’s what’s happened is on every conceivable front, there’s been this corralling of different components of our environment that are disruptive to our mitochondria.

Ari: Got it. Okay. Since we have to wrap up, I’m sure that we can still talk for many more hours, Morley. Do you want to finish by mentioning maybe two or three to-do items, two or three practical things that you want to recommend people to start doing more of in addition to the list of things that we just went over to talk about doing less of as far as vitamin D and multivitamin, especially like typical synthetic multivitamins and synthetic B vitamins and iron supplements, zinc supplements, vitamin C supplements, vegetable oils, highly processed carbs, things like that? What about two or three practical takeaways that you can leave people with of things that they should do more of?

Morley: Wherever possible, eat an ancestral diet. Eat foods that your ancestors would recognize, in season, colorful, locally grown, things like that. Second, we all have emotional demons that affect our physiology. Profound impact, unresolved emotional issues, fears that we have. The level of chronic fear on this planet now three years later is still very significant. I strongly encourage people to do emotional release work, whether it’s EFT, or EMDR, or emotion code, but release your fears that you’re broken. Very, very important to do that.

I think the third thing that I would encourage, well, I guess I’ll say four things. Third would be, please get into a routine of regular blood donation for postmenopausal women. And guys, you can do it every quarter. Women who are still experiencing their menstrual cycle, you probably could do it a couple times a year in addition to your monthly blood loss. The fourth item that I would recommend, Ari, is believe in the innate intelligence of your body. The part that we’ve not known about is that the nutrients that empower and really activate our innate intelligence are the focus of the root cause protocol.

Basically, all I did was just dust off mother nature. I don’t take pride of authorship that, oh, I’ve discovered this. I just found the natural metabolic pathways and what are the nutrients that are critical to make those pathways work. I think it’s important for people to truly believe in their body’s ability to heal itself because so many people who are chronically ill are convinced they’re broken. That comes back to the demons.

The thing is, the body is amazing. It is incredibly intelligent, and it has a wisdom when it is properly fed, back to the ancestral diet, but the focus of the RCP to make sure that the nutrients are working in synergy to optimize energy and to clear the exhaust. I think that’s how I would put someone up.

Ari: Beautiful. Morley, I have thoroughly enjoyed all of our interviews, but I think this one the most. I thank you so much for all of your time, and I suspect we’ll probably be talking again in the near future. I think you probably have more things that come to mind that you want to share, and we’ll do a fourth episode maybe in a month or two or three or six, who knows?

Morley: Yes, that’s great. I appreciate that. I want you to know, what I’ve enjoyed most is you have a rigor, and a discipline, and an objectivity to let’s get to the kernels of truth as best we can. I really appreciate your measured focus to make sure that your followers understand not just your understanding of this, but to make sure they understand it, even in the context of the controversial nature of it. I really value your thought process to bring that about.

Ari: Thank you so much, Morley. I really appreciate the kind words. Thank you for noticing that. I certainly try to do that and I appreciate you pointing it out and bringing attention to it. Thank you so much, my friend. It’s really been a great pleasure getting to know you and learning from you.

Show Notes

Chronic inflammation anemia versus iron deficiency anemia (02:50)
The prevalence of iron deficiency anemia misdiagnosis (13:37)
Why iron is problematic for health (16:56)
The healthy levels of ferritin (23:23)
How curcumin affects copper and iron levels (34:12)
Uric acid and blood sugar (40:04)
Is supplementing vitamins healthy? (53:30)
How blue light and EMFs affects health (1:28:50)


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