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In this episode, you will learn about iron dysregulation and hemochromatosis.  

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About My Guest

My guest for this episode is Dr. Christy Sutton.  Christy Sutton, DC's interests in asking why health problems occur, what the root causes are, and what are the safest and most effective solutions to health problems are the foundation of her writing, teaching, and clinical practice.  Her personal health struggles, and her desperation to find answers to her own serious health problems surrounding Crohn’s and Celiac disease have led her down the alternative healthcare path and to look for ways to find and avoid genetic landmines.  Her first book "Genetic Testing: Defining Your Path to a Personalized Health Plan" and its corresponding "Genetic Detoxification" report were the precursors to creating the Labrogenomics educational webinars and to writing her upcoming book "The Iron Curse".  Her book "The Iron Curse", inspired by diagnosing her husband and many patients with hereditary hemochromatosis and iron-related health problems, takes a deep dive into hemochromatosis and other iron-related disorders.  Her husband's hemochromatosis led to liver problems and likely led to the development of a pituitary tumor that caused Cushing's syndrome.  From her experience as a clinician, she has discovered that there is an epidemic of undiagnosed and untreated hemochromatosis, and this epidemic is being driven by myths, misperceptions, and a failure on the part of the medical community that should be diagnosing people with hemochromatosis; a disease that is easy to screen for, prevent, diagnose, and treat.  "The Iron Curse" course and upcoming book are powerful tools for ending the epidemic of undiagnosed and untreated hemochromatosis, and they give people the information they need to diagnose, prevent, and correct iron-induced damage.

Key Takeaways

  • What is hemochromatosis?
  • What factors affect iron regulation?
  • What genes are involved in iron overload?
  • What is hepcidin?
  • What tests should be done to explore iron regulation?
  • What is ferroptosis?
  • Can iron play a role in neurodegenerative conditions?
  • What is the connection between high iron and diabetes?
  • Can iron play a role in autoimmune conditions?
  • Does iron impact the endocrine system?
  • How might high iron be involved in elevated uric acid levels or gout?
  • When might nitric oxide supplementation be considered in relation to iron levels?
  • How does iron act as fertilizer for infections?
  • Does iron play a role in hypercoagulation?
  • How does iron impact mitochondria?
  • What are the key components of the Iron Curse Protocol?
  • What are the different types of anemia?

Connect With My Guest



The Iron Curse Workshop

Interview Date

April 13, 2023


Transcript Disclaimer: Transcripts are intended to provide optimized access to information contained in the podcast.  They are not a full replacement for the discussion.  Timestamps are provided to facilitate finding portions of the conversation.  Errors and omissions may be present as the transcript is not created by someone familiar with the topics being discussed.  Please Contact Me with any corrections.  


[0:00:02] ANNOUNCER: Welcome to BetterHealthGuy Blogcasts, empowering your better health. Now, here's Scott, your BetterHealthGuy.


[0:00:14] ANNOUNCER: The content of this show is for informational purposes only, and is not intended to diagnose, treat, or cure any illness, or medical condition. Nothing in today's discussion is meant to serve as medical advice or as information to facilitate self-treatment. As always, please discuss any potential health-related decisions with your own personal medical authority.


[0:00:34] SCOTT: Hello everyone, and welcome to episode number 183 of the BetterHealthGuy Blogcasts series. Today's guest is Dr. Christy Sutton. The topic of the show is The Iron Curse. Dr. Christy Sutton's interests in asking why health problems occur, what the root causes are, and what are the safest and most effective solutions to health problems are the foundation of her writing, teaching, and clinical practice. Her personal health struggles and her desperation to find answers to her own serious health problems surrounding Crohn's and Celiac disease have led her down the alternative healthcare path and to look for ways to find and avoid genetic landmines.

Her first book, Genetic Testing: Defining Your Path to a Personalized Health Plan and its corresponding Genetic Detoxification Report were the precursors to creating the Labrogenomics Educational Webinars and to writing her upcoming book, The Iron Curse. Her book, The Iron Curse, is inspired by diagnosing her husband and many patients with hereditary hemochromatosis and iron-related health problems. It takes a deep dive into hemochromatosis and other iron-related disorders. Her husband's hemochromatosis led to liver problems and likely led to the development of a pituitary tumor that caused Cushing Syndrome.

From her experience as a clinician, she's discovered that there's an epidemic of undiagnosed and untreated hemochromatosis and this epidemic is being driven by myths, misperceptions, and a failure on the part of the medical community that should be diagnosing people with hemochromatosis, a disease that is easy to screen for, prevent, diagnose, and treat.

The Iron Curse course and her upcoming book are powerful tools for ending the epidemic of undiagnosed and untreated hemochromatosis and they give people the information they need to diagnose, prevent, and correct iron-induced damage. Now, my interview with Dr. Christy Sutton.


[0:02:33] SCOTT: I am excited today to dig into a complex and often overlooked topic in chronic illness, namely iron dysregulation. Dr. Christy Sutton's made iron-related conditions a major focus of her work and of her teachings. I had the opportunity recently to take her five-part course, The Iron Curse, and I'm very excited to learn more from her in our talk today. Thanks so much for being here, Dr. Christy.

[0:02:56] DR. SUTTON: Thank you. Thanks for having me.

[0:02:59] SCOTT: Talk to us about your personal journey that led you to exploring iron dysregulation, both from a high iron, or hemochromatosis perspective, but also, a low iron, or type of anemia perspective.

[0:03:14] DR. SUTTON: Yeah. Personally, I have dealt with low iron more – I've never had a high iron issue, because I have Crohn’s, I have part of my small intestine removed, I have Celiac disease, I'm a female that menstruates and I gave birth to a child. I have many, many risk factors for low iron and that's been something that I have definitely had to struggle with. When I first started practicing, I wanted to really make sure I wasn't missing this in other people. I got really good about running iron panels, which is where I started to slowly pick up on, oh, there is a lot of low iron out there, but there's also this issue where some people have high iron.

Then I really got good at it after I diagnosed my husband with hereditary hemochromatosis. It was a process getting him officially diagnosed, which was also a learning process. But him getting diagnosed with that and then me writing my first book about genetic testing and having a chapter on that hemochromatosis gene and really starting to dig into not just looking at the labs, which are very important and most people are not running all of the labs, they should be running for an iron panel. But also, the genes, those two, I think, always need to go hand in hand and we're not anywhere near there. But to me, this is a necessary stack for healthcare, because every doctor every day talks about iron. It's just a ubiquitous common problem.

[0:04:48] SCOTT: If I remember correctly, your husband's situation was pretty extreme in that he had significant liver issues, that he potentially related to the iron overload, developed a pituitary tumor and Cushing syndrome. I mean, these are not minor things that we're talking about.

[0:05:04] DR. SUTTON: Right. Yeah. Well, it was interesting because my husband, he just has one of the low, considered low risk HFE H63 genes, which by many people’s standard, it's impossible to get hereditary hemochromatosis with that genotype, which is a myth that I'm trying to put to rest. By modern standards, he's called mild. His hematologist diagnosed him as a mild hereditary hemochromatosis.

It was already causing liver damage. He had high liver enzymes. They were getting up into the 80s and the 90s by the time we finally got it fully diagnosed and treated. I consider it to be very significant. It was interesting to go through this process where the gastroenterologist was not really that concerned about them being that high, I guess, because they just see so many really, really sick people, like the bar is so low, they were not that worried about it. Everybody said, “Oh, we caught this so early. It's so mild.” But it was causing serious liver damage. Since then, his liver enzymes have come down, because the iron's lower and the damage has been healed up. Hopefully, we're doing our best.

I believe, I'll never have a doctor tell me this, but I believe that my husband's Cushing's disease, which is he has a pituitary tumor that causes him to secrete too much ACTH, which causes him to have high cortisol. I believe that his Cushing's disease was caused by, if not largely accelerated by the fact that he had undiagnosed high iron for so long. The reason I believe that is because high iron is very hard on certain parts of the body, especially the anterior pituitary gland, which is where his tumor is. It can cause tumors.

[0:06:54] SCOTT: Let's talk first about hemochromatosis. What is it? How common is it? Then what are some of the symptoms that might lead someone to maybe even just considering the potential for high iron? What happens when we have high iron in the body and are there specific organs, or tissues that are most impacted by elevated iron levels?

[0:07:14] DR. SUTTON: Yeah. Hemochromatosis is a disease where you have too much iron. It can be called iron overload. It can be called hereditary hemochromatosis. It just depends on if you have the genes. If you have the genes, it's going to be hereditary hemochromatosis. If you have those genes, you're more likely to develop hemochromatosis, because you're absorbing more iron just genetically. But you don't have to have those genes. There's a lot of people that develop high iron for just environmental reasons. They just develop high iron as a result of diet, lifestyle, age. They have iron overload non-hereditary hemochromatosis.

Regardless of if it's hereditary or non-hereditary, the end result is that you have too much iron and it's creating a lot of damage and oxidative stress. It's like rusting the body from the inside on a cellular level. It's extremely dangerous. Iron has an affinity for specific parts of the body, although eventually, it can just destroy the whole body. It tends to go for certain organs first. It goes for the liver first. The liver is where iron is largely stored, so the liver is often the first organ to get damaged. Then it also has a high affinity for the gonads, the testes and the ovaries. It'll create infertility type issues, hormonal imbalances there.

It'll go for the brain, creating neurodegenerative issues, Alzheimer's, Parkinson's, depression, bipolar, etc. It'll go for the pituitary gland in the brain creating hormonal issues. It'll go for the pancreas, creating blood sugar issues, diabetes, and then it'll go for the heart creating cardiovascular disease. Really, it goes for the whole body, the skin, everything. There's no cell that's left undamaged by the time iron overload has really had its ability to really set in.

[0:09:16] SCOTT: Just a few minor things, it sounds like.

[0:09:18] DR. SUTTON: Just a few minor things. Yeah, no big deal.

[0:09:23] SCOTT: In your course and in your upcoming book, you talk about some of the environmental factors that affect our levels of iron. What are some of those demographics, or environmental factors that we might want to think about?

[0:09:37] DR. SUTTON: Age is a part of that, because as we age, we're going to be accumulating more iron. People who don't have the hemochromatosis gene, they tend to be lower in iron when they're younger. Just because when you're young, you're using more iron, you're often on a calcium rich diet. High calcium diet is another factor, because calcium binds to iron, making you more likely to not absorb iron. Alcohol is a huge contributing environmental factor. If you consume alcohol, then you're going to absorb more iron. You're also going to create more damage to your liver on top of the extra iron that's already damaging the liver.

Diet, of course, if you eat a high iron diet, you're more likely to absorb more iron. Menstruation, if you're losing blood through menstruation, that can be a huge amount. That's the equivalent of potentially donating blood at least once, or twice a month. Or a GI bleed. That's a huge factor. Also, people can lose a lot of blood through a GI bleed. There's supplements that you take. Some can increase iron absorption, like vitamin C. Others can decrease iron absorption. Really, everything that we do has this effect on our iron more or less.

Iron is so important in our health that our immune system really tries to control it, because even if you get an infection, that's going to influence your iron levels. Your body knows that that iron is a fertilizer for many infections. It's going to get the iron out of the blood to try to protect you from infection really being, given the fertilizer that it needs.

[0:11:19] SCOTT: Another one that you mentioned in the course that people may not recognize is birth control pills, also can affect levels of iron. Do you want to comment on that as well?

[0:11:28] DR. SUTTON: Yeah, yeah. That's a really important one. Birth control pills, there's a lot of different factors involved in that. One is that estrogen, the estrogen in birth control pills can actually increase iron absorption. Also, when you're on a birth control pill, often you're taking it maybe because you have heavy menstrual cycles. Generally, when people take a birth control pill, they don't bleed as much as they normally would with a normal natural menstrual cycle. They bleed less, which is a huge factor. You're not losing as much iron.

Then in addition to that, a lot of times the placebo pills for the week off when you're supposed to be “menstruating,” when you're bleeding on a birth control pill, those often have iron in them. There's a lot of different factors. I have seen young girls and teenage girls that develop high iron, because they have this hemochromatosis gene and then they're given birth control. Then it accelerates the damage.

The irony is when these people get properly diagnosed and treated, often their menstrual problems get better without the birth control, because often, it was the high iron that was messing up their menstrual cycles anyways, because it destroys the pituitary gland and the ovaries.

[0:12:51] SCOTT: We'll see how many times we can squeeze the word irony in, no pun intended. Oftentimes, I think people have the perspective that many are low iron and high in copper. Others suggest that many are high iron and low in copper. I'm wondering, how often do you see high iron compared to low iron and then low copper compared to high copper in your patient population?

[0:13:18] DR. SUTTON: Yeah. You can have all of the above. Everybody's different. I think it's dangerous to make gross generalizations. I think, really, the most important take home point for me is we all need to be looking at iron and copper very closely. One of the things about looking at copper is that if there are certain genetic diseases, like Wilson's disease where you actually appear to have low copper, or low ceruloplasmin on blood work, but that's because you're not able to excrete it from your liver like you should be able to.

The copper and the ceruloplasmin ends up just getting stuck in your liver and you get copper damage in your liver, and it can also create damage in the brain for the same reason. It gets in the tissue. It's hard. We really need to be looking at the genes for those copper diseases and the ceruloplasmin and the copper and the red blood cell copper. Then we need to be looking at a full iron panel. This is even something that I struggle with. I'm very comfortable with the iron piece. Now the copper piece is harder, because it's really much more complicated from a lab perspective. I think that's where we really need to just accept that we're going to have to get better about testing.

One of the limiting factors for me is the lab that I love to use, it doesn't automatically include the red blood cell copper and the serum copper and the ceruloplasmin. The lab that I love to use, it doesn't even offer the red blood cell copper. Now I'm in a situation where, okay, I'm going to have to order for multiple labs. Then I also want a hair analysis on top of that. I always look at those iron genes, but I'm having a hard time finding a place to check the copper genes. I think this is where this is going to go in the future with really better answering your question. I think these are good questions and I'm sorry, I don't have better answers. Certainly, we need to do better. We need to be really careful about just saying, okay, you were low in copper, or low in ceruloplasmin, which ceruloplasmin is a copper-dependent enzyme that when you're low in copper, your ceruloplasmin can go down. You can also have that Wilson's disease, where you get low in ceruloplasmin because you're just not excreting it. We just have to do a better job.

Just because you're low, doesn't mean that you're actually low in copper. You could give somebody copper and make them sick. I hear a lot of people saying, “Oh, iron deficient anemia, that's a low copper situation.” I think that's an oversimplification, too. You can have copper deficient anemia where you're low in copper that creates an iron deficient anemia. I think to just automatically assume that is dangerous.

[0:16:13] SCOTT: From a genetic perspective, what are the requirements to be diagnosed with hemochromatosis? You alluded to this earlier, but if we, for example, look at the HFE genes in order to meet the technical criteria for hemochromatosis, do we need to have two copies of both the C282Y and the H63D? Or can we be heterozygous, or have one mutation and still have an issue? Talk to us a little about what this HFE gene is and how common mutations are that might set the stage for iron overload?

[0:16:48] DR. SUTTON: Yeah. This is really an important question. I even have a chapter in my book called The Carrier Myth. We must end the carrier myth. Basically, the carrier myth is this idea that you have to have two hemochromatosis genes to have hereditary hemochromatosis. There's two hemochromatosis genes that are well documented in the literature. It's not a question as to if they can create high iron. It's been well documented. The two are what you just said, the HFE C282Y and then the HFE H63. There is this myth that you have to have two of those. Meaning, you either inherit two from one parent, or one from two parents, but you have to have at least two to actually have hereditary hemochromatosis.

That is a really dangerous myth, because as I just said, my husband developed hereditary hemochromatosis with just one. What I find most common, and this is something that I look at closely, because I'm looking at so many people's genes and labs, I find that almost everybody that I diagnose with hereditary hemochromatosis has just one gene. The reason for that is because that's the most common genotype in the population, to have one or the other, like either one C282Y, or one H63. Now, the more genes you have, the higher your risk. If you have two instead of one, your risk will be higher, but it is less common to have two than to have one.

Really, the way that you diagnose hereditary hemochromatosis is based on labs and genes. The way you diagnose hemochromatosis period is based on blood work. If you do blood work and you see that somebody has a high iron saturation, high ferritin, that's hemochromatosis, regardless of them having that gene. Everybody should be screened for these genes anyways, but especially anybody that has a high iron. If they have anything out of range high, or questionable and functional range, then you need to always get those genes to see, is that what's driving this high iron? Because if that is what's driving this high iron, then it's not likely to get better on its own and it's likely just to get worse and worse with time. Unfortunately, most people that have hemochromatosis are not diagnosed for a very long time, which allows the high iron to just wreak havoc on your body for decades, for some people.

[0:19:30] SCOTT: Some of the things that I noted from taking your course was that about 31% of the global population has at least one of these HFE genes. Then when we have this HFE propensity to iron overload that we can absorb as much as three times more iron when we have these genes. The C282Y, my understanding is that that one is maybe more significant than the H63D and also is involved in lowering hepcidin. Talk to us about hepcidin. What is it? How do the levels of hepcidin in the body impact our iron levels and our iron storage?

[0:20:10] DR. SUTTON: Hepcidin is the brakes on absorbing iron. Really, when you have hereditary hemochromatosis, meaning that you have one of those genes, then you are genetically programmed to make less hepcidin, which is the brakes on iron. If you genetically make less of those brakes, then you're going to absorb more iron.

Like you said, there is a higher risk with the C282Y, because that absorbs more iron. Apples and apples being equal, let's say identical twins that are eating the identical diet, the C282Y will absorb more than somebody with the H63. Okay, but like I said, there's so many environmental factors, so we can't just look at genes.

Yes, back to your question about hepcidin. Hepcidin is the brakes on the iron. In a normal person that doesn't have the hemochromatosis gene, when iron levels start to increase, then the liver will start to produce more hepcidin to decrease iron absorption. Now, in somebody that has hemochromatosis, they just simply cannot create as much hepcidin, so they cannot stop the absorption of iron like they should. Then that creates just this inability to shut down the absorption.

There's a lot of environmental factors that can affect hepcidin, too. Like, if you have any type of liver disease, that's going to decrease hepcidin. Alcohol consumption decreases hepcidin. Testosterone decreases hepcidin. There's just so many different environmental factors that can really decrease hepcidin. Many of them are pathological, meaning they're not good for you. However, there are environmental factors that can increase hepcidin. If you get an infection, then that can cause you to have more hepcidin. That creates anemia of inflammation.

The immune system, it knows that iron is potentially a big problem when it's trying to get rid of an infection. Because like I said, it's fertilizer for a lot of different infection, pathogens. The immune system will basically tell the liver to make more hepcidin whenever you're sick, so that you can get the iron out of the blood and then put the iron in the liver and the spleen and in the macrophages, okay. And in the intestinal lining as well. Basically, what happens is you end up increasing ferritin, because the immune system is saying, put it in the storage unit, get it out of the blood. It puts all of the iron into the storage places and it gets it out of the blood. Then you end up with this massive increase in ferritin that is not necessarily caused by high iron. It's simply caused by inflammation, or an infection, which is why ferritin alone is not the best marker for iron. It can also be inflammation.

[0:23:22] SCOTT: It's obviously very complicated. But more simplistically, high iron levels lead to an increase in hepcidin, which then helps to lower the iron level in the blood. If we have low iron, that leads to a reduction of hepcidin, which then results in an increased iron level in the blood, correct?

[0:23:42] DR. SUTTON: Yes.

[0:23:42] SCOTT: Okay. Great. When we think about MTHFR as an example, we can supplement with methyl  B12, or hydroxy B12, or the right types of folate, folinic or 5-methyl folate and essentially, optimize, or some people use the term bypass our less than optimal genes. Is there a way to influence the expression of the HFE genes themselves? Are there epigenetic influencers that we know of that impact how those genes express? Or is everyone that has the same HFE gene combination at equal risk?

[0:24:19] DR. SUTTON: The more HFE genes that you inherit, the higher your risk. I can't think off the top of my head of any way to decrease the expression of the HFE genes. I think you're going to – your body is going to make the HFE enzymes to the same potential, regardless of what you do more or less. Really, the best way I think to modulate somebody that has those HFE genes is what I outlined in The Iron Curse, which is really using the environmental factors diet, nutrition, lifestyle to basically modulate hepcidin.

Because as we just said, really the whole story of hemochromatosis gene is a hepcidin story. These people don't genetically make as much hepcidin. If we can increase hepcidin and decrease iron, then we can really maybe save some of these people from having high iron and iron-induced damage.

[0:25:35] SCOTT: In your course, you talk about supply and demand for iron. How much iron do we need in a day to support our health before it starts to potentially become health negating, or moves from a nutrient to a toxin? How do those HFE genes impact our absorption of iron? What are some of the scenarios where we might lose iron at a higher rate and thus, maybe do need more supplemental iron?

[0:26:00] DR. SUTTON: Supply and demand is really a huge part of the story. The amount of iron that one needs varies and the amount of iron that one consumes and absorbs varies greatly. People that have the hemochromatosis gene. They can absorb three to five times more iron than somebody without the hemochromatosis gene, like eating the same diet. Of course, you also have to look at digestive health. If you have a poor digestive system, you're not going to be absorbing things as well, so there's a lot of factors there. You have to look at how much blood are they losing?

As far as just the supply, meaning, how much are you actually consuming and absorbing, on average, what we need is about 1.8 milligrams of iron a day, which means most people, they absorb around 1 to 3 milligrams of iron a day. We lose around 1 milligram of iron a day just through urine, blood, sweat, the skin. Some people say we don't lose iron, but that's wrong. We do. We lose around 1 milligram a day, which is very low.

The point I'm trying to make here is the body tries to keep iron very tightly regulated. Meaning that it doesn't want to really lose very much at all, because we need it for survival. Many people throughout history have died of low iron, even today. The United States, there are tons of iron deficient people out there. This is really why the hemochromatosis gene is so successful in society is because iron deficient anemia has hurt so many people and killed so many people that this gene that allows you to absorb exponentially more iron is very advantageous.

Assuming that you're not losing a lot of iron, if you're only absorbing 1 to milligrams a day, that's fine. If you have a GI bleed, or if you're pregnant, you could be losing up to 7 to 10 milligrams a day, which is huge. If you have the hemochromatosis gene, you could be absorbing 7 to 10 milligrams a day. My point is there's a lot of different factors. That's why it's so important to look at the labs and the genes and the environmental factors.

[0:28:24] SCOTT: These HFE genes really are a blessing and a curse.

[0:28:28] DR. SUTTON: They are. They are. Historically, this gene basically traveled through this Celtic Viking ancestral lineage. Then, that's why it's so common in the Caucasian Northern European population, especially in Ireland after the potato famine, they got really, really common. It's traveled throughout the whole world, because globalization, just people travel. It's not just in Caucasians. That's another myth. Basically, our ancestors lived during this time when it was common for people to die of iron deficient anemia, either from blood loss from an injury, or menstruation, or just not being able to eat enough iron, because there's a famine. This was really, I considered a warrior survival gene that has been extremely successful. It's just in the wrong environment, which many people now live in, because our ancestors didn't have a McDonald's on every corner and they didn't have iron supplements to take.

They were iron deficient anemic much more than high iron. I just don't think they dealt with a lot of high iron issues, because of their environment. Whereas we now, have iron fortified foods and iron's everywhere and sedentary population, which is going to – the more you're sedentary, the less iron you're going to lose. There's just a lot of factors that are making this an Achilles heel now.

[0:29:59] SCOTT: I will admit that I don't even know where the nearest McDonald's is.

[0:30:03] DR. SUTTON: Good for you.

[0:30:06] SCOTT: You mentioned earlier that iron can be very oxidative, that it's like rusting from the inside. Are those with lower antioxidant status, lower glutathione status, are they more likely to have negative consequences as a result of the iron overload?

[0:30:25] DR. SUTTON: Absolutely. Glutathione is basically, one of the antidotes to oxidative stress. It's like the bulletproof vest to protect you from the free radicals that oxidative stress creates. Iron, it creates a lot of oxidative stress. You watched The Iron Curse, in that I cut an apple in half. One apple, I put lemon juice on it and the other apple I don't. Of course, the apple that has lemon juice is not all brown. Then the apple that doesn't have lemon juice is all brown. That's oxidative stress. That's like, the electrons are getting stolen from the apple, which is creating a chemical reaction, which is causing damage.

If you take that step by step by step in the future, that is what ultimately causes aging degeneration and cancer is that oxidative stress. Iron is like putting gasoline on a fire that is already burning. It's just creating more oxidative stress, more free radicals, more little bullets shooting at you. Now, like I said, glutathione is that protective shield. There's many protective shields in the antioxidant world, but glutathione is a really important one, especially for the liver. We really need to make sure, everybody needs to make sure they have plenty of glutathione, but especially people that have high iron. Because if you have high iron and low glutathione, then you're going to be really accelerating serious irreversible damage, which I think is probably what happened in my husband, honestly, because he tends to have – he has these genes that cause him to have low glutathione, and I think this is a common situation.

Then if you compound that, not just the low-glutathione, high-iron, but remember what I said about how iron really is bad for the liver, because it stores in the liver as ferritin, well, that's also where a lot of the glutathione is used and created, and so you're basically depleting the glutathione in your liver by having high iron. It's this vicious cycle that's just harmful and creates more ferroptosis.

[0:32:35] SCOTT: Let's talk a little bit about some of the testing. If we look at thyroid, for example, many times people are just getting a TSH test and then conclusions are drawn. Walk us through in the iron world, serum iron, iron saturation, TIBC, UIBC and ferritin, and what those potentially tell us, why we need to really look more broadly than just the basics?

[0:32:58] DR. SUTTON: The full iron panel that is absolutely necessary as a minimum to diagnose hemochromatosis, really, you need a CBC, which is going to be looking at hemoglobin, hematocrit, red blood cells, white blood cells, the MCV, the red blood cell size. You need the CBC, but you also need the full iron panel, which doctors are really good about ordering CBCs. They're not so great about ordering the iron labs, which is ironic, because we live in a world where people have either high, or low iron, almost everybody. They'll often maybe order a serum iron, or they'll order a ferritin, but rarely do they order all of them and you really need all of them.

What's in a full iron panel is the TIBC, UIBC, serum iron, ferritin, and iron saturation. The most sensitive markers for high iron are really the ferritin and the iron saturation. Iron saturation is just looking at a formula of basically, looking at serum iron and TIBC. It's important that you're looking at all this in a fasting state, because if it's not fasting, then your serum iron can go higher. The truth is your serum iron is like a snapshot. It's a fasting glucose. It can be all over the place. Whereas your hemoglobin A1C changes a little bit slower. The serum iron is the fasting glucose that just can go up and down, depending on how much iron you ate. Whereas, the iron saturation and the ferritin, those are going to more, so be likely to reflect the history, the long-term history of how much iron is really accumulating and building up.

Then the TIBC and the UIBC, the TIBC is basically looking at how much transferrin do you have to transport iron around the body. When the tissues are saturated with iron and they're like, “I'm done, that's enough. Stop.” Then it's going to shut down the transferrin, which are the little planes that are flying the iron to and from throughout the body. When iron's high, the body says, “No more planes, no more transferrin.” Then the TIBC goes down, because it doesn't want to bring any more iron to the tissues.

That's a confusing thing for a lot of people, is they see a low TIBC and they think, “Oh, my iron must be low.” It's actually the opposite. Low TIBC, the planes are not – the body's not sending out the planes to take iron to the tissue. Low UIBC means that those planes don't have – they don't have enough unsaturated iron binding capacity. There's not enough seats on the planes. The seats are all full, because the iron, there's too much iron, so the seats are all full. There's no open seats.

The UIB, the unsaturated iron binding capacity, the seats that are open, those go down also. Low UIBC, low TIBC happens with high iron. Whereas, with low iron, you'll see more high TIBC, high UIBC.

[0:36:13] SCOTT: What do you consider to be a healthy ferritin level that stored iron? I've seen some suggest the range of 50 to 75, maybe as ideal. What are some of the risks of high ferritin? Then where does hemosiderin come into the discussion?

[0:36:29] DR. SUTTON: If you end up building up enough ferritin, then that ferritin will degrade into hemosiderin. The body can only store so much ferritin. At some point in time, it plateaus, and it's like, we can keep accumulating iron, but we're going to have to accumulate it as hemosiderin, because our storage capacity as ferritin is maxed out. It's like a hoarder. We've put the iron everywhere we can in the closets, and now it's just going to start spilling over out of the closets into the hemosiderin.

The hemosiderin is really quite dangerous, not just because it creates a lot of oxidative stress and damage, but it's dangerous because it has an unlimited potential to store iron. Whereas ferritin plateaus, and it's not going to be able to store any more iron. Hemosiderin can just keep going forever until it kills you. The average person stores around 6 to 10 grams of iron, depending on the person. Somebody with hemochromatosis, they can store as much as 50 grams of iron, so that's exponentially more.

By the time you get to 50 grams of iron, you have just tons of hemosiderin. Now, the problem is we can't actually measure hemosiderin, just like we can't measure hepcidin and routine clinical testing. These are more academic tests that are getting done. This is not a lab that you can ask your doctor to order, and they'll just be able to order it, like the iron panel, or the CVC, or those things that are just routine. That's what hemosiderin is.

As far as a healthy range for ferritin, that's a really good question, and I think that's where you really have to look at the whole picture. My husband recently had some blood work done, and I just told him, “Ask your doctor to order the iron test,” because he only sees the hematologist once a year now, which I don't think is enough. But his endocrinologist was ordering labs, because he still has that pituitary tumor. His endocrinologist, I said, just order the iron labs, just so that we can see where you are.

He had a high iron saturation, like 56 iron saturation. High iron, serum iron, but his ferritin was only 60. Not the most uncommon situation. What was interesting about it is that the hematologist still wanted to go ahead and remove some blood, just to get the iron levels down. I think when it comes to these iron issues, the doctors who are really trained to treat it, they realize that it's a case-by-case basis. While they try to be scientific, at some point in time, you have to make a judgment call like, okay, this, I know this person has this gene, I know that their ferritin is in a pretty darn good range, but the iron is getting higher and we need to do something about it to lower it.

Many people end up with just an obvious high ferritin, and then that's not a question at all. Many people don't get diagnosed till their ferritin’s in the thousands. But for managing hemochromatosis, the hematologist really often like to keep it within a very narrow range. When they were first trying to get my husband's iron down, like in the initial days of getting diagnosed, they wanted his ferritin below 50. I was concerned he was getting too low. That is something that often happens as people go from one extreme to the other. I think 50 to 75 is a really good range for people for ferritin. But you can't just say, “Oh, my ferritin's good,” and then not look at the other ones.

If you're showing high iron, especially with the hemochromatosis gene, and you have a high iron sat and high iron serum, then you still need to be working on supporting lower levels of iron, because you have too much iron that's just getting to the tissues.

[0:40:43] SCOTT: How accurate do we feel blood testing is for looking at this iron picture? Just the example would be, we do a lot of thyroid testing using blood, but that doesn't necessarily give us any reflection of what's happening at the level of the cell.

[0:40:59] DR. SUTTON: I think it's fairly accurate. You're right. We don't have an exact idea of what's exactly going on at the cell, just because we don't have the blab marker maybe for that. I think it's fairly accurate, especially when you start looking at it in combination with the genes. You can really start to assume safely that if somebody has anything that's out of range high with those genes, that it's a result of high iron and not a result of just inflammation. Although, inflammation and infection can certainly play a role in that, because like I said, inflammation and infection, they just drive that ferritin through the roof and can affect the amount of iron in the blood.

There's limiting factors, which is why I think when you see something that's out of range, iron-wise, you need to retest multiple times, because they change. Then you need to know, was this just an anomaly, or is this a pattern that's going in the wrong direction just because of high iron?

[0:42:07] SCOTT: How can people check their HFE genes to see if they have this potential to accumulate iron? Is that part of a standard 23andme and something that's easily accessible? Or do you then have to take the raw data and run that through some other reporting application? What's the easiest way to know your HFE status?

[0:42:26] DR. SUTTON: Most people at this point in time have done 23andme. I will just either get their raw data and run it through the Genetic Detoxification report, if they haven't paid for the health reports. Actually, I do that anyways, just because I want to get additional information on top of those hemochromatosis genes. The hemochromatosis genes are definitely included on the 23andme reports, if you pay for the health reports. If you don't pay for the health reports, if you just do the ancestry, then you can get the genes through that downloading the 23andme data and uploading it to the Genetic Detoxification report.

Now, having said that, the 23andme reports that they give you are very misleading. If you've seen the 23andme health reports, then it'll say, hemochromatosis gene, not likely to have hemochromatosis. Low risk. But they inherit. It's not like there's no variant. They have the gene. It's just they're saying, very low risk, when that's – That goes back to the carrier myth. My husband and my daughter have the hemochromatosis gene. Their genetic reports say not at an increased risk, because they're misinterpreting the meaning, and that's because of this myth that you have to have, too, which is so dangerous.

[0:43:45] SCOTT: If someone has their raw data from 23andme, you mentioned this Genetic Detoxification report, is that something they can then do through your website, or do they have to be a patient of yours?

[0:43:54] DR. SUTTON: Yes. No, anybody can run the Genetic Detoxification report. They can either go to Dr. Christy Sutton, or Genetic Detoxification. Either place will get you there. It's just $30 for the Genetic Detoxification report, which has a lot of different genes. Then those genes, most of them go along with my first genetic book, although I've added a mini after that genetic book was printed. I need to go back and update the book eventually.

[0:44:25] SCOTT: You used the term ferroptosis earlier, this iron-induced cellular death. What are the factors that must be present for ferroptosis to occur? What is it?

[0:44:36] DR. SUTTON: Ferroptosis is a programmed cell death that happens whenever you have a lot of iron combined with low free radicals. What happens is the iron creates a lot of damage to the cell membrane. It will damage the lipid molecules on the cell membrane. Because you don't have enough glutathione and antioxidants to decrease the free radicals from high iron, then you create so much damage to the cell membrane that the cell basically decide that's going to kill itself, instead of create cancer and create more health problems.

The ferroptosis itself is a problem, because you're destroying what should be healthy tissues. It is something that the body's doing for a reason. If you remove that underlying reason of high iron, high oxidative stress, low glutathione, low antioxidants, then the ferroptosis will stop. It is a pathological process that is dangerous and creates massive damage to wherever it occurs. The body does it for a reason. The body is trying to preserve itself. It's just sometimes, it has to make sacrifices, because it's in a bad situation.

[0:46:10] SCOTT: You mentioned that iron can affect the brain. Can high iron contribute to cognitive issues, brain fog, dementia, maybe even Alzheimer's disease? How commonly would you suspect high iron could be a contributor in that population?

[0:46:26] DR. SUTTON: I think it's very common. Just from what I've seen and granted, I don't have a couple thousand-person, double-blind placebo trial, or meta-analysis. Just from what I have seen, I think it's very common. In The Iron Curse, I have those genetic combinations that if you have this gene and this gene, be careful because this is a bad combination. Well, even if you don't have the hemochromatosis gene, if you just have high iron in combination with a, like Alzheimer's gene, then that's a very high risk, because the high iron is going to basically, create more damage to the brain. Then that's going to accelerate your risk for neurodegenerative diseases, like Alzheimer's, Parkinson's, etc.

[0:47:19] SCOTT: How about the connection between high iron and blood sugar, or even diabetes?

[0:47:23] DR. SUTTON: High iron will create damage to the pancreas, specifically the beta insulin-producing cells of the pancreas are largely damaged. It can create both type one and type two diabetes. Then the irony of that is that basically, as your blood sugar goes up, that further suppresses your hepcidin, which means that you're going to absorb more iron, which means that you're going to have more iron to damage your pancreas and create insulin resistance and diabetes.

[0:47:58] SCOTT: You snuck in that word, irony again.

[0:48:02] DR. SUTTON: If it was a drinking game.

[0:48:04] SCOTT: Is there a connection between high iron and autoimmunity? It's been my opinion for a long time that autoimmunity is the result of either infection, or environmental toxicant. Wondering if that toxicant, or toxin driving autoimmunity could be something as seemingly benign as iron? Have you seen correlation to autoimmunity conditions in your high-iron patients and do those conditions resolve with iron reduction strategies?

[0:48:33] DR. SUTTON: There is definitely clinical data that shows that high iron, hereditary hemochromatosis, iron overload increases the risk for autoimmune diseases. The risk is of course, going to be higher if you have a family history of autoimmune diseases. That's not surprising at all. It can create pretty much any autoimmune disease. However, the most common autoimmune diseases that it is going to create are autoimmune hepatitis, which is where your immune system attacks your liver, which makes sense because if your immune system is attacking your liver, it's because the liver is damaged largely.

If you have high iron, then you're going to have a lot of liver damage and inflammation, and then your immune system is going to go to try to heal it up. In the process of it trying to heal it up, because you have all that inflammation, it might lose tolerance to itself and start attacking the liver. That's a common issue, as far as autoimmune diseases.

Autoimmune thyroiditis, Hashimoto's is in the literature as well. Then there is good research that high iron will accelerate the demyelination and seen in MS, which is very serious. There are certain things that can protect from that, some of the antioxidants. High iron, I would include that in my autoimmune trigger, like the triggers, which my autoimmune triggers that I think about are stress, toxins, which I would include iron to be a toxin, whether it's a chemical, or a heavy metal, or iron. Too much iron is toxic. Not enough, that's not good, but too much is toxic. Stress, toxins, infections, gut type issues are big accelerators for autoimmune diseases.

Now, the high iron also creates leaky gut dysbiosis and digestive issues. You see that a lot with people that have hemochromatosis. If you have leaky gut digestive issues from high iron, then you're going to even further increase your risk for an autoimmune disease, because it's very clear that if you have all this gut dysbiosis, leaky gut, you're going to have more inflammation, more of a risk for losing tolerance to your immune system.

Lowering iron certainly will help decrease one's risk for, I think, triggering an autoimmune disease. Lowering iron will certainly help decrease the inflammation and the stress on the body, which will then help your body to be less likely to have a flare up and a problem. What I don't see is I don't see somebody that maybe has positive antibodies that has already developed an autoimmune disease, and then they lower their iron and those antibodies just go away completely. Maybe they get lower, just because the immune system is not working as hard, there's less inflammation. But I don't think once you've turned those autoimmune genes on from high iron, I don't think they're as likely to just turn off. Maybe in some cases, they can, but that's not something that I see a lot. I think at that point in time, you really have to manage the flare-ups and try to create as much immune tolerance as possible.

[0:51:50] SCOTT: You mentioned the iron's impact on the pituitary, on the gonads. I want to talk a little bit about the impact of iron on our endocrine system. Does iron directly reduce testosterone, for example? Can addressing iron overload normalized testosterone and might giving supplemental testosterone in some of these high iron scenarios create more problems?

[0:52:16] DR. SUTTON: Definitely, when you talk about testosterone. Testosterone is going to decrease when you have high iron, because that iron destroys the testosterone producing cells in the testes. As a result, you're going to produce less testosterone. One of the unfortunate problems with people that have hemochromatosis is they get diagnosed with testosterone being low, but not the high iron. This creates an issue, where they end up treating the symptom rather than the cause, which is a dangerous situation, because if you give somebody testosterone, that's going to decrease hepcidin, increase iron absorption. Not only does it do that, but it also accelerates the risk for them having high hemoglobin and high hematocrit and high red blood cells, which increases the clotting risk that one already has when they have hemochromatosis. It's really dangerous.

The fact that people are testing for and giving testosterone and not routinely testing for iron issues is really disturbing to me, but that's the world we live in largely is what I find. If somebody has iron damage, which causes low testosterone, and then they lower the iron back to normal, then their testosterone may go back up, if they haven't had so much damage, so that it's already caused irreversible damage to their testes.

If that's the case, then they will have put out the fire, but the damage is already done, and they may never be able to make as much testosterone as they'd like, because those cells are just destroyed. It just depends on the person. But in those cases, those people may actually need a small amount of testosterone, but only give the testosterone once you've fixed the iron issue and watch very closely to make sure that that doesn't create future high iron issues, because it can.

The other issue with the endocrine system that's really unfortunate and very sad, and I think a really serious issue that I'm seeing clinically is infertility in females. Now it can cause infertility in men too, by just decreasing testosterone and sperm quality and sperm count. In females, you'll see a low AMH, which is the anti-mullerian hormone, which is a hormone that's made by the ovaries. When that gets low, then that's a sign that one's fertility is low and their ovaries are not as healthy as they should be, and they're not going to have as high of a chance of getting pregnant naturally.

This is certainly, I think, a very serious issue that is another reason why we really need to be diagnosing this early, early, early. Young girls need to get tested for this. My daughter, who's nine-years-old, she developed a high ferritin from the hemochromatosis gene. Her doctor only ordered the lab, because I asked her to and then didn't even report the finding to me. I've been lowering it and we're about to recheck it. My colleague's daughter at the age of five was diagnosed with hereditary hemochromatosis. My point is that these things can happen really early if you have these genes. They're not getting tested for and diagnosed, because pediatricians are not running these labs.

[0:55:31] SCOTT: Gout is a common condition that we think of is more an arthritic type presentation as people get older. Is there a connection between high iron and levels of uric acid or gout? Might uric acid also be a blessing and a curse?

[0:55:49] DR. SUTTON: High iron definitely causes uric acid to go up. Then when you lower iron, it will lower uric acid. That's one reason that people with high iron tend to have more gout attacks, but they also get what's called pseudo gout, which is where their misdiagnosed as having gout, but it's actually just high iron induced damage to the joints. The blessing of it is that like I said, the body's really intelligent and it's just trying to survive underneath bad circumstances. Iron's a really bad circumstance that's creating a lot of damage. The body creates more uric acid, because uric acid is this wonderful antioxidant. It's just trying to put out the fire of high iron with the uric acid.

Then once that fire is put out, because the iron's lowered through whatever mechanism, you lower it, then the uric acid can naturally go down, because now the body's like, “Okay, we don't have to have the fire hose anymore.” The uric acid can go back down, which means you're going to have fewer gout flares.

[0:56:56] SCOTT: Can I think then of the uric acid is essentially an antioxidant that is protecting us from the oxidative stress of the high iron levels?

[0:57:06] DR. SUTTON: Yes, certainly. Or any other oxidative stress, whether it's iron, or some chemical, or whatever. It's protective.

[0:57:17] SCOTT: Endothelial health is a popular topic these days, particularly in the pandemic era. Nitric oxide supplements seem to be becoming more popular, more prevalent. Would we want more, or less nitric oxide in someone with iron overload? What's the connection between iron and nitric oxide, or iron and endothelial health? Do we want to attempt to increase nitric oxide if our iron levels are still high?

[0:57:44] DR. SUTTON: When you have high iron, it will cause endothelial dysfunction, meaning it'll cause low nitric oxide, because it just damages those endothelial cells. If you have damaged endothelial cells, then you're going to have less nitric oxide. If you have low antioxidants, because you have high iron, you're going to have less nitric oxide, which means you're not going to have that wonderful ability to dilate and get blood circulating through the arteries and the capillaries, which is a problem.

Having said that, the iron does decrease nitric oxide. I do discuss increasing nitric oxide in the protocols and The Iron Curse protocols, but I do that at the end of the – it's towards the end. you've already lowered the iron, before you're boosting the nitric oxide. Hopefully, just by lowering the iron and increasing antioxidants, that nitric oxide naturally goes back up. If it doesn't go back up like you'd like from lowering iron and boosting antioxidants, then at that point in time, you could consider boosting nitric oxide, maybe exogenously with nitric oxide, or something.

I would not recommend one take anything to boost nitric oxide supplement-wise, until they have lowered their iron and increased their antioxidants. Because if you have high nitric oxide, it will react with the free radicals, which the iron creates, and then that will create peroxy nitrates, which create a lot of tissue damage and vascular damage and increase your risk for heart attack and stroke and whatnot.

[0:59:30] SCOTT: I want to come back to the iron is like fertilizer for infections conversation. Many of our listeners are dealing with chronic infections, like Lyme disease, or Borrelia, which is not iron dependent as I understand, but others as well, Bartonella, Babesia, many of the herpetic viruses, like EBV, herpes zoster, cytomegalovirus and so on. How does iron impact these chronic infections? Are there specific infections that you see more concerning when there are higher iron levels?

[1:00:03] DR. SUTTON: Borrelia, like you said, that is manganese dependent, not iron dependent. Yeah, which is interesting.

[1:00:10] SCOTT: I didn't know you were an expert on Borrelia, but I'm impressed.

[1:00:12] DR. SUTTON: I’m not. I have written about it in The Iron Curse, because when you're studying iron, it comes up. Actually, the fact that the Borrelia can use manganese instead of iron is one way that is so good at evading the immune system. The immune system ties iron as the main thing, as far as the minerals go to really influence. If it can't influence that iron to get over the infection, which it can't with the Borrelia, then it just doesn't have the tools it needs, so that's a big problem. Now, on a case-by-case basis, I can't say that I have research to show that every single pathogen and how iron affects it, but it is most every pathogen. The literature specifically isolates Borrelia. It doesn't really isolate any other pathogen as far as iron goes. It says, Borrelia is unique, because it's manganese dependent and not iron dependent. I haven't read that about other things. It might be out there. I just haven't read it yet.

The literature, what I see infections are much worse when you have high iron, whether it's viral, or bacterial, or parasitic. It's just, you have this breeding ground for iron. Then your immune system’s often suppress, just because the high iron can suppress your immune system, too. Really, more so the issue is it's this breeding ground for high iron, which is why they saw with COVID, the people who had high iron were much more likely to have more long COVID, or really acute, awful, deadly COVID situations when they had high iron.

[1:01:58] SCOTT: Let's talk a little bit about the hypercoagulation. Again, very common in the chronic illness community, those people dealing with lime and babesia, mold illness, now long COVID and those types of conditions. It sounds like, iron has an additional impact then on the potential for blood clots, or hyper-coagulation. In these people that have hyper-coagulation is iron one of the key things you would be looking at to reduce their hyperviscosity?

[1:02:27] DR. SUTTON: Absolutely. Because when people have hemochromatosis, it doesn't just affect their iron. It also increases their red blood cells, their hemoglobin, hematocrit in many cases. That will increase the viscosity of the blood. It's going to make it thicker. That's largely, because when you have too much iron, the body is trying to find a place to store it. One place that it will store it is the hemoglobin. The body makes more hemoglobin. That becomes a serious risk just for clotting. That's not the only mechanism that iron increases clotting risk. It also increases clotting risk, because it creates so much inflammation and oxidative stress and vascular damage, which are all also – and decreases antioxidants, which are all additional risk for clotting.

[1:03:18] SCOTT: Mitochondrial dysfunction, the ability to make ATP is so critical in these chronic conditions. ATP is the energy currency of the body. Talk to us a little bit about how iron impacts the mitochondria. Can it actually get into the cells and directly impact energy production?

[1:03:38] DR. SUTTON: Absolutely. It is very clear that when you have too much iron, it's going to cause mitochondrial dysfunction. It's going to create all this oxidative stress, which is going to damage the mitochondria. Now, mitochondria are pretty good at creating antioxidants, because they live in a high oxidative stress environment, because creating ATP and running that electron transport chain, it creates a lot of oxidative stress. They have evolved to create massive amounts of antioxidants.

One of those antioxidants is melatonin, but it's not the melatonin that you get at night. This is the circulatory melatonin. The circulatory melatonin is which is made when you go out in infrared light. That creates massive amounts of melatonin, which creates less oxidative stress. Lowering the iron is going to decrease oxidative stress and help the mitochondria, but also making sure that you go out in infrared light and then get that circulatory melatonin, which is 95% of the melatonin that the body makes is made in the mitochondria. Only 5% is made by the pituitary, the pineal gland, which is sub-cellular melatonin. Yeah, any antioxidants, whether it's melatonin, or glutathione, or increasing superoxide dismutase, all of those are going to help decrease mitochondrial dysfunction.

[1:05:10] SCOTT: Melatonin is definitely my personal drug of choice and have used it for many, many, many years. Does high iron lead to an increased risk of cancer? You've already hinted at this before. Is that any type of cancer, or is it more cancers where iron is specifically deposited in high amounts, such as the liver, for example, maybe the pancreas you mentioned as well?

[1:05:33] DR. SUTTON: Once you've developed high iron, it's going to basically find your Achilles heel and go after that. Of course, if somebody has a genetic increased risk for breast cancer and then they add high iron to that, they're probably more likely to get breast cancer. All things being considered, of course, the organs that are the most sensitive to high iron, like the liver, the pancreas, the brain – I think my husband's pituitary gland was caused by high iron – the pituitary tumor was caused by high iron. Certainly, the liver.

People that have high iron are much more likely to have liver cancer, like 200 times more likely to have liver cancer. The research, I mean, is pretty clear, it's just about any cancer, whether it's ovarian, testicular, pancreatic, prostate, blood cancer, bladder, it just, the list goes on, melanoma, skin cancer. When you create a lot of DNA damage from high iron, creating oxidative stress, your risk for cancer goes up, period.

[1:06:41] SCOTT: Now, we get to talk about some of the interventions, potential treatment options. What are some of the key interventions you might consider in those with iron overload? We're going to go deeper into these, but walk us through at a high level, your Iron Curse five-step protocol.

[1:06:56] DR. SUTTON: The first step is lower the iron by removing blood, okay. If you can, that's the caveat, if you can, removing blood is a very efficient way to lower iron. Not everybody can remove blood, because some people, they have low hemoglobin and high iron, and then they can't remove blood, or they have low red blood cells and high iron. Then they're just going to create another issue by removing blood. Blood removal is the most common tool used to lower iron in the people that are treated for high iron. It is a powerful tool, and it's a good tool.

I think it's unfortunate they're not using all the other tools that I have in the Iron Curse protocols. The current standard recommendations for people that have hemochromatosis are blood removal as prescribed. Avoid vitamin C supplements, low iron diet. Avoid red meat and shellfish. That's the big things they recommend. They don't talk about any of the other steps, which I include. Removing blood is the first step in the protocols.

The second step is, of course, dietary. The third step is supplement nutrition, and then lifestyle, and then – just lifestyle protocols. Then the last one is preventing ischemia reperfusion injuries. The whole goal of all of that is to basically, lower the iron as quickly as possible, not just in the blood, but in the tissues, and prevent it from going high again, and heal up the damage and prevent the damage, which a lot of – they don't talk about that in the normal allopathic medical world.

[1:08:39] SCOTT: Let's dig in just a little bit to each one of these steps. You were talking about giving blood, therapeutic phlebotomy, I think is another term for that, donating blood to essentially reduce levels of iron. Is that something that people commonly would specifically go and say, “I'm doing therapeutic phlebotomy for iron reduction”? Or do they, if they are able to, do they just go donate blood and that's the way they approach it?

[1:09:05] DR. SUTTON: The blood donation rules are changing. It used to be that if a doctor told you to donate blood and you had hemochromatosis, then you couldn't just go donate blood. Maybe you could go to a blood donation center, but you'd have to have a doctor prescribe it, write a prescription. That has since changed at most places. Now, you can donate blood if you have hereditary hemochromatosis.

Assuming you don't have some other reason that you can't donate blood, like being in an area that has malaria, having a transmittable infection disease, the blood donation piece is a powerful piece. Now, in some cases, if just a random person goes and tries to donate blood, because their doctor tells them to and they tell the blood donation center that they might say, “No, we can't do this.” But the same random person could go and donate blood if they didn't tell the blood donation center that, “My doctor told me to do this,” which is totally asinine, but that is how it is in many cases.

Blood donation, people that donate blood regularly tend to live longer, and that's largely because they're unintentionally, or maybe on some cases, intentionally lowering their iron. Having said that, I have seen a number of people that I don't want them to be donating blood. It's not going to make their life longer. They're making themselves anemic. Blood donation, in my opinion, is a medical procedure and should never be done without thorough blood work before. I'm not saying it's not good. It can be wonderful, if necessary. But I think just the idea that anybody can go willy-nilly donate blood is misleading. Ideally, everybody should get an iron panel, or CBC before they do that.

[1:10:55] SCOTT: Since so many people listening to this podcast are dealing with chronic Lyme disease, please do not donate blood if you have Lyme and related co-infections. If you're doing this for purposes of iron reduction, make sure that the blood is disposed of.

What are the key dietary changes that one might need to think about if they're dealing with iron dysregulation? You mentioned red meat, shellfish. Are there other key things that we should think about?

[1:11:19] DR. SUTTON: Red meat and shellfish are the highest sources of heme iron, which heme iron is much more absorbable than non-heme iron. Non-heme iron is found in vegetables, fruits. Heme iron is only found in animal protein, animal products. Non-heme iron is found in the vegetarian, vegan type, non-animal products. This is why people that eat a vegetarian vegan diet are much less likely to have high iron. I think they tend to have a lot of other issues that are maybe not a high iron issue, but certainly, you'll have a lower risk for high iron if you're not eating animal products, because there's no heme iron in them. That's why it's a fallacy for people to believe like, “Oh, I'm getting plenty of iron from spinach.” Oftentimes, I'll tell people, “Well, you're anemic.” They say, “Well, I eat a lot of spinach.” I’m like, “Well, you don't absorb much iron from spinach. It doesn't work very well.” Diet plays a role.

If you do have really high iron, then you probably need to be careful about the amount of iron you're consuming in your diet, until you get things under control. Personally, I feel you can eat those foods once your iron's in a normal range. If you follow the other steps in the Iron Curse protocols to help decrease iron absorption and remove extra iron. But everybody is different.

[1:12:56] SCOTT: What are some of the key nutrients that can help in those that are dealing with iron overload? Are these binding iron and improving excretion? Are they increasing hepcidin? Are they helping in other ways? What are the more common key interventions that come to your mind for iron overload?

[1:13:13] DR. SUTTON: The most common one that I've used is curcumin, which is an extract from turmeric. Curcumin binds to iron and it removes it. Then there's other ones that bind to iron and remove it silymarin and alpha lipoic acid and green tea extract. All of them have their pluses and minus to them. I think you have to use them specifically, depending on the person in their situation. Then there's other things in the protocols that increase hepcidin. They lower iron absorption by helping the body make more hepcidin. Because remember, the whole problem with hemochromatosis is that you don't make enough hepcidin.

The things that increase hepcidin are things like quercetin, berberine, and even melatonin. Then there's other nutrients that, like the glutathione and the vitamin E and things, where that's really just to boost those antioxidants, so that you don't have as much damage and ferroptosis. Then there's additional things to help heal up the damage, like phosphatidylcholine and whatnot. This is where I list a lot of different things in the Iron Curse protocols. I don't think everybody needs to take everything. I just think the more you know, the more tools you have, the better you can create a personalized plan for yourself.

[1:14:40] SCOTT: I had my tablespoon of phosphatidylcholine this morning. Thank you for that mention as well. If high iron depletes glutathione, which we know that it does, and supplemental glutathione potentially helpful for buffering, or mitigating that oxidative stress, is N-acetylcysteine, or NAC as a precursor for glutathione equally appropriate?

[1:15:03] DR. SUTTON: Surprisingly, there is some research that shows that people that have high iron that take NAC, N-acetylcysteine, they actually can create more problems in the short run. They think that's because the NAC might increase iron absorption, although I haven't been able to find a real definitive answer on that. That's the hypothesis. That is not the case with glutathione. For the people that do have high iron, they might want to just do more the glutathione route, the acetyl glutathione, or the liposomal glutathione, and wait until their iron levels are lower before doing the NAC.

Now, there is some research that if you give an iron chelator with the NAC, then that helps negate the problems that the NAC can cause. If you don't know that, you might just give somebody NAC, and then that could create more problems.

[1:16:03] SCOTT: You mentioned the term chelators. Are there specific chelators that can be helpful with directly reducing iron, for example, DMPS, or DMSA, or EDTA? Do any of those play a role in this conversation?

[1:16:16] DR. SUTTON: No. When I said chelators, I was thinking more curcumin, or silymarin, or alpha lipoic acid. That's not what they used in the research. But when they do research that compares curcumin to prescription chelators, curcumin does just as well, if not better, without the side effects.

[1:16:39] SCOTT: Let's talk a little bit about vitamin A and also magnesium in iron regulation. I was a little unclear, because vitamin A is said to increase hepcidin, which would then decrease serum iron. I've also read that vitamin A can increase the absorption of iron. When might we want to, or not want to supplement vitamin A?

[1:17:04] DR. SUTTON: Vitamin A, when you're low in vitamin A, especially when you're low in vitamin A combined with low copper, but low vitamin A, that will create low ceruloplasmin. Ceruloplasmin, like I said, is this enzyme that needs copper. It actually allows you to get the iron and attach it onto the transfer in molecules. You transport the iron from the digestive lining to the transferrin via the ceruloplasmin. Then once on the transferrin, the iron can go throughout the tissues. When you have low vitamin A, you're not going to have as much ceruloplasmin. Then when you don't have as much ceruloplasmin, then you can't get the iron. Iron is not going to be absorbed as well. Then it's not going to be transported as well, which is going to create an issue where you're going to see more iron loading in the tissues, but also lower iron, potentially in the blood, because it can also – low vitamin A can create high hepcidin, and high hepcidin can decrease iron absorption.

[1:18:29] SCOTT: It seems somewhat clear now why I was a little confused about the vitamin A.

[1:18:34] DR. SUTTON: It's confusing. It really is confusing.

[1:18:37] SCOTT: Then how about magnesium? My understanding is the magnesium can help to minimize some of these iron deposits, or deposition of iron in specific organs.

[1:18:46] DR. SUTTON: Magnesium will compete with the iron, especially with the absorption of iron. People that are low in magnesium tend to have more iron deposits in their tissues. Also, low magnesium can increase the risk for hemolytic anemia, which can also create more iron, high-iron overload type issues.

[1:19:06] SCOTT: I want to talk a little bit about binders. We commonly use binders to help bind to and maximize excretion of heavy metals, or chemicals, or pesticides, or mycotoxins. Is there a role for using binders in an iron reduction protocol?

[1:19:24] DR. SUTTON: Anybody that's using binders needs to research those specific binders they're using and see, are they binding to iron? Are they binding to calcium? What are they binding to, to make sure that you may not be creating unintended problems? I know, I've certainly seen in people that we're doing a lot of detoxing, they started getting a lot of side effects from low minerals, muscle cramps and not sleeping well and things like that. I think it's important to do the research on what binders you're taking.

I don't have a lot of personal experience that I can tell you with specific binders for detoxing, lowering iron, but I think it could happen. I haven't been able to find really good research on just in general some of these binders. How do those affect iron? I think it's just where you need to check. You need to be checking iron really closely, too. Certainly, binders can bind minerals and they can bind iron, which could be good if they have high iron, or it could be bad if they're low.

[1:20:34] SCOTT: How often is supplemental zinc, or supplemental copper part of your Iron Curse protocols? When you do use copper, do you generally use the Cu1, or bioavailable forms of copper, or the Cu2, which is more commonly what we see in a lot of different supplements?

[1:20:52] DR. SUTTON: I tend to use the copper glycinate, which I think is the Cu2. I've started using copper more within the last year. I'm certainly using it with people that have high iron, because the people that have high iron often will end up with low ceruloplasmin, and then that'll create more issues. Also, if you eat a really high iron diet, that iron's going to potentially compete with the copper absorption in the first part of the small intestine and then you're more likely to become low in copper, which can create a vicious problem.

[1:21:36] SCOTT: How about any value of supplemental zinc in these Iron Curse protocols?

[1:21:40] DR. SUTTON: Zinc certainly can play a role and people that are low in zinc are potentially more likely to have iron induced damage as well. Zinc can also compete with the copper for absorption in the small intestine. I think, you have to be careful with using too much zinc, because zinc can bind to copper and then you end up with a unintended low copper consequence, which could then create more iron issues.

[1:22:11] SCOTT: Let's touch on step four of your Iron Curse protocols, which is lifestyle. How does lifestyle impact iron dysregulation? Are there direct lifestyle changes that impact iron? Or are these more holistic things that anyone should be doing anyway?

[1:22:28] DR. SUTTON: Exercise. Now, that's a big deal, because you're going to lose more iron whenever you exercise, which is why people exercise a lot often become low in iron. Often, many of these people that have hemochromatosis, they get winded very easily. You might need a lower iron before you exercise. Exercise, stress reduction, trying to really maybe not go to high altitude locations, while you are dealing with the acute high iron, because if you have high iron and then you go to high altitude, then that can create more iron induced damage. Exercise and sweat daily. Get really adequate sleep, because when your body's very stressed out – we always need plenty of sleep. If you're not sleeping, then that's just going to accelerate the damage.

Try to limit alcohol, reduce toxin exposure, like pesticides, try to eat organic, that type of stuff, because the toxins are going to further decrease hepcidin in the liver. Also include in there, heal the blood brain barrier, which really probably comes down more to a nutritional piece, because if you really want to heal the blood brain barrier, you're going to have to look at the nutrition piece.

[1:23:44] SCOTT: You mentioned sweating. I know people have major different levels of heavy metals in sweat, in those people doing infrared sauna, do we know if there's any value in infrared sauna in an iron reduction protocol?

[1:23:57] DR. SUTTON: I haven't been able to see any research on that, but I do include the infrared sauna in the Iron Curse, because if you're getting that near infrared radiation, then you're going to be able to increase more melatonin in the mitochondria. Then that extra melatonin in the mitochondria is going to decrease the mitochondrial dysfunction, which is a risk of high iron. Just in general, decrease oxidative stress. That's that part of it. The other part of it is sweating is going to – you lose a ever so slight amount of iron in sweat. If you're maybe not healthy enough to go really exercise and work up a sweat, then maybe you can work your way up to a sweat in a sauna.

[1:24:45] SCOTT: The last step, or step five in your Iron Curse protocol is looking at reperfusion injury. Talk to us about what that is and what we might do to avoid additional problems as a result of that.

[1:24:58] DR. SUTTON: Reperfusion injuries is something that's talked about as much as it should be. When somebody has a stroke, or a heart attack, or even if they have a surgery where blood supply is restricted to a part of their body, like if they get an organ transplant, so a lot of people that end up with liver damage from high iron may need to get an organ transplant. Okay. When they actually do that surgery, there's often a period of time where there's not enough oxygen going to the liver, or if you're having a stroke, you're not getting enough oxygen to your brain. That's the ischemia part. The ischemia part is not getting enough oxygen.

Then what happens is after the ischemia has occurred, then the body overcompensates by sending this massive amount of blood to the area, which creates this secondary trauma, which is filled with lots of oxidative stress and damage. The analogy that I use is the ischemia, the original injury, whether it was a stroke, or the heart attack, or the surgery, or the traumatic brain injury, which you can also get ischemia reperfusion injuries with traumatic brain injuries, concussions, then that's like getting in the car accident. Then the reperfusion injury is like, you flew out of the car and because maybe you were not buckled up or whatever. It's like the second injury on top of the first one.

My hope is that people, by doing the Iron Curse protocols and really honing in on their health, they can be less likely to have these ischemia injuries in the first place, whether it's a stroke, or heart attack, traumatic brain injury, whatever, also, be less likely to have that reperfusion injury. You have a window of time after you have an ischemia injury, where you can massively increase antioxidants to basically, you have the small window of time where you can protect yourself from that secondary trauma, but you have to really be on top of it. It's basically massive amounts of antioxidants as soon as possible at the moment of the injury.

[1:27:25] SCOTT: In our last few minutes together, I want to talk about the opposite side of the coin, which is low iron, or what most people think of as anemia. We know with iron associated anemia, you've mentioned that females more susceptible, those without HFE genes, more susceptible, vegan vegetarian people more susceptible. Maybe what people don't always recognize is that there's many types of anemias that are not associated with low iron. Talk to us a little bit about the different types of anemia that listeners should think about.

[1:27:58] DR. SUTTON: There's copper deficient anemia, which if you're low in copper, you're actually more likely to be low in iron, because you need copper for the enzyme that helps you absorb iron in the intestines, which is called hephaestin. Copper deficient anemia creates iron deficient anemia, although many people can have iron deficient anemia without copper deficient anemia, especially people that lose a lot of blood. Then there's anemia from other nutritional deficiencies, like from maybe low B vitamins, which can create megaloblastic anemia, where the red blood cells get too large.

You can have non-megaloblastic anemia, which is where the red blood cells are too large, but it's not from being low in B vitamins. It's usually from alcohol abuse, liver damage. You can have aplastic anemia, which is where high iron can cause megaloblastic anemia. It can cause non-megaloblastic anemia by causing nutritional deficiencies. It can cause, especially the aplastic anemia, because basically, the bone marrow gets damaged, and then you're not creating as many red blood cells, and then you get low red blood cells. You can have iron loading anemia, which is where you have too much iron, but you're still anemic at the same time, because you have low red blood cells, low hemoglobin. That can sometimes also be called iron avidity.

You can have hemolytic anemia, which is where your red blood cells are getting damaged much faster than they can be repopulated, and then that actually can create high iron with low red blood cells, low hemoglobin. You can have anemia of inflammation, which is where we talked about that, where you have high hepcidin from maybe an infection or inflammation, and then your ferritin goes high, but the iron gets low, and you're not absorbing as much iron over time, because the hepcidin’s high. Those are the major anemias that I cover in the Iron Curse.

[1:30:01] SCOTT: We're not going to touch on all of those in great detail in the rest of our conversation, but would you say that the vast majority of anemias are iron-associated, or not necessarily?

[1:30:11] DR. SUTTON: Yeah. The ones that I see.

[1:30:14] SCOTT: Can we have both hemochromatosis and anemia at the same time? Is the risk for iron-associated anemia lower in those people that do have these HFE mutations and is low iron more common in those without any HFE issues?

[1:30:31] DR. SUTTON: Anybody that has one of those hemochromatosis genes is less likely to have iron deficient anemia. But I'll tell you, I see females that are pregnant with low iron all the time that have those genes. Pregnant females with the hemochromatosis gene, they get low in iron a lot. If you ever see somebody that's low in iron that has a hemochromatosis gene, then you need to figure out what's going on, because they're bleeding somewhere most likely, either a GI bleed, or really heavy menstrual cycle, or they're pregnant, or something is going on that's really depleting them rapidly.

But yes, they're less likely to have high iron. Anybody that doesn't have those genes, like myself are at a higher risk for low iron. That's the hemochromatosis gene part. You can have hemochromatosis and anemia at the same time. That would be an iron-loading anemia, where you might have high ferritin, high iron saturation, high serum iron, low TIBC, low UIBC, but you'd also maybe have low red blood cells, low hemoglobin, which would then be the anemia part. Or, you might have large red blood cells, which are the MCV, which would be another type of anemia, megaloblastic anemia.

[1:31:59] SCOTT: Earlier, you talked about the fact that the highly absorbed iron is not found in plants, that it's found only in animal products, that heme iron. In those that need supplemental iron, what is your favorite type of iron?

[1:32:13] DR. SUTTON: Ferrous peptonate, iron supplements that have animal-based iron in them. Whenever I see an iron that is vegetarian-based, I just do not feel like it works as well, which is a problem because a lot of people that become low in iron are vegans and vegetarians, and then they want to take a vegan vegetarian iron. It just is a hard situation.

The fact is that any heme iron is going to work so much better. Of course, I always like people to get their iron from their diet, but many people do need iron supplements. Whenever I do give iron supplements, I like ferrous peptonate.

[1:32:56] SCOTT: Is ferrous peptonate, is that a heme iron?

[1:32:58] DR. SUTTON:  The ferrous peptonate that I use is yes. It's from animal protein.

[1:33:05] SCOTT: We talked a little bit about vitamin C. Is vitamin C something that potentially would help with iron absorption in those people with low iron? Maybe in an iron associated anemia, or low iron anemia might be a good thing, but might be something we want to be more cautious about in those people with high iron, or hemochromatosis?

[1:33:25] DR. SUTTON: This is a hard one, because on one hand, vitamin C is this wonderful, inexpensive antioxidant. But if you take vitamin C, it's going to increase iron absorption, especially if you take vitamin C with an iron-rich meal. It's going to increase iron absorption. It actually increases non-heme iron absorption the most. I think that if you're going to take vitamin C, just try to take it with the low – If you're high in iron, then try to take vitamin C away from the iron foods you're eating, or just get your vitamin C through your diet, which I don't think I would never tell somebody, don't eat vitamin C-rich foods, because I think that's an awful recommendation, especially with somebody with high iron, because they really need those antioxidants and the vegetables and fruits.

I think you really do need to be careful. People with the hemochromatosis gene might really want to think twice before they supplement with high doses of vitamin C, a 1,000 or 2,000 milligrams a day.

[1:34:36] SCOTT: Which so many people have been doing in the past three years, because of the pandemic, right? That's something to think about.

[1:34:40] DR. SUTTON: I think a lot of the issues we're seeing now, it's predictable that now everybody – there's this whole group of people that want to talk about copper, because during the pandemic, everybody was taking zinc. It's like, okay, well, maybe we just made our population copper deficient, because everybody was taking zinc and all these things and have we just created these other issues. That's a tangent.

[1:35:06] SCOTT: You've talked about the fact that the heme iron that comes from animal products is more desirable than the non-heme iron that comes from plant-based products. Is the non-heme iron biologically active? Do we still get benefits from it? Or is only the heme iron what we really get some health benefits from, assuming we don't have too much?

[1:35:29] DR. SUTTON: We get benefits from both. The difference is absorption. Absorption happens in the intestines. The heme iron from animal products is better absorbed than the non-heme iron in the fruits and vegetables. You're not going to be absorbing as much. But once you do absorb it, it's all the same. It's just a matter of getting it into your blood.

[1:36:02] SCOTT: I know you've dug into this area a lot. I'm wondering if you use any homeopathic tools for dealing with either high, or low iron. For example, ferrum metallicum, or PEKANA FERRODONA, or maybe cell salts. Do any of those have a role in trying to increase iron regulation?

[1:36:19] DR. SUTTON: I don't have any personal experience with it. It's a great question. I just haven't experimented with it, or really dug into it research wise, but I think it's a great question.

[1:36:31] SCOTT: I will put the link in the show notes to where people can find you, where they can find your course, the Iron Curse. Tell us a little bit about The Iron Curse book. When is that going to be available and where can people find it?

[1:36:43] DR. SUTTON: The Iron Curse book will be out in the next couple months in 2023. The book mirrors the workshop, educational workshop, both of those, you can find at ironcurse.com and of course, it'll be available at Amazon. If you go to ironcurse.com, then you'll get some other good things there. The workshop is available now and it is similar to the book. It mirrors it, but there are some things that I go into greater depth in the workshop, which is five videos. The book, of course, I can go into more depth as far as the research and some of the details.

[1:37:25] SCOTT: Yeah, it's a great course. I mean, it's at least six hours. I learned more about iron than I ever knew I needed to know. Definitely, for those people that are dealing with these types of issues, or practitioners that ideally would want to learn more about this to help their patients, the Iron Curse protocols and Iron Curse course are fantastic. Looking forward to the book as well. My last question is the same for every guest and that is, what are some of the key things that you do on a daily basis in support of your own health?

[1:37:54] DR. SUTTON: I have Crohn’s. My things are, I have to really spend more of my time and energy focused on my diet than most people, because it's a digestive autoimmune disease. I also have part of my small intestine removed, and so I have to just really be very careful about diet, avoiding the foods that I know are problems for me. I have to be careful about sugar, gluten, dairy, just generally. I have to spend more time and energy on that.

Then being a working mom, and that's in the health care field, it's not for a lack of knowledge that I don't get my personal time and do the things that I need to do. It really is sometimes more of a just time management type issue. I have relied more and more on having a coach to help me, whether it's a personal trainer, or somebody that's an accountability partner to make sure that I'm getting my workouts in and doing what I need to do.

My husband's wonderful, as far as his sleep hygiene and he helps me with that. Then I've also found that I really have to take some days not being in the office to just get my life together. Unfortunately, because I'm in this busy season with promoting the book and getting the book published and everything, I've been infringing on my days off more than I'd like to. I think that's a really important thing. I'm going to claw back and protect those days off for what life brings up and I need to take care of. I think that's really important, build in some free time and then have good relationships with friends, or family, or loved ones, or whatever. I'm fortunate to have a wonderful daughter and husband and good friends. Those are key.

[1:39:45] SCOTT: Wonderful, wonderful. Such a great discussion. I think you busted a lot of myths. You shared a lot of ironies with us as well. Thank you so much, Dr. Christy Sutton, for the work that you're doing with the Iron Curse and looking forward to the book as well. I just appreciate you and all that you're doing.

[1:40:02] DR. SUTTON: Thank you so much.

To learn more about today's guest, visit DrChristySutton.com. That's D-R-C-H-R-I-S-T-Y-S-U-T-T-O-N.com.


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