Episode #183: The Iron Curse with Dr. Christy Sutton, DC

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Hello everyone and welcome to episode number 183 of the Better Health Guy Blogcast series. Today's guest is Dr. Christy Sutton and the topic of the show is the iron curse. Dr. Christy Sutton's interest 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 youg Path to a Personalized Health Plan and its corresponding Genetic Detoxification Report were the precursors to creating the Labro Genomics educational webinars and to writing 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's 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. And now my interview with Dr. Christy Sutton. I am excited today to dig into a complex and often overlooked topic in chronic illness, namely iron dysregulation. Dr. Kristi 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 am very excited to learn more from her in our talk today. Thanks so much for being here, Dr. Christy.

Thank you. Thanks for having me.

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.

Yes. So 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, you know, menstruation traits, and I, you know, gave birth to a child. So I have many, many risk factors for low iron. And that's been something that I have definitely had to struggle with. And then. So when I first started practicing, I wanted to really kind of make sure I wasn't missing this in other people. And I got really good about running iron panels, which is where I kind of started to slowly pick up on, oh, you know, there is a lot of low iron out there, but there's also this issue where some people have high iron. And. And 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, you know, a learning process, but him getting diagnosed with that and then, you know, 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, 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, that this is a, this is a necessary step for healthcare because every doctor every day talks about iron. It's just a ubiquitous common problem.

And 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, right?

Yeah. So. Well, it's. It was interesting because my husband, he just has one of the low considered low risk HFE H63 genes, which by many people standard you. It's impossible to get hereditary hemochromatosis with that genotype, which is a myth that I'm trying to put to rest. But he, by modern standards, he was. He's called mild. Like, his hematologist diagnosed him mild hereditary hemochromatosis. So it was already causing liver damage. He had high liver enzymes. You know, they were getting up into the 80s and the 90s. By the time we finally got it, you know, fully diagnosed and treated, I consider 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. You know, 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, you know, the iron's lower and the damage has been healed up. You know, hopefully we're doing our best, but 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. So I believe that his Cushing's disease was caused by, if not largely, you know, accelerated by the fact that he had undiagnosed high iron for so long. And 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, and it can cause tumors.

So let's talk first about hemochromatosis. What is it? How common is it? And 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?

Yeah. So 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, and they just develop high iron as a result of, you know, diet, lifestyle, age, and they have iron overload. Non hereditary hemochromatosis. But regardless of if it's hereditary or non hereditary. The end result is that you have too much iron and it's creating oxidative, it's creating a lot of damage and oxidative stress. It's like rusting the body from the inside on a cellular level. And so it's extremely dangerous. And iron has an affinity for specific parts of the body, although eventually it can just destroy the whole body. But it tends to kind of go for certain organs first. So it goes for the liver first. The liver is where iron is largely stored. So the liver is often, you know, the first organ to get damaged. And then it also has a high affinity for the gonads, like the testes and the ovaries. So it'll create, you know, infertility type issues, hormonal imbalances there. It'll go for the brain, creating neurodegenerative issues. Alzheimer's, Parkinson's, depression, bipolar, et cetera. 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, you know, cardiovascular disease. But it really goes for the whole body, the skin, you know, everything. There's no cell that's left undamaged by the time iron overload has really had its ability to really set in.

So just a few minor things.

It sounds like just a few minor things. Yeah, no big deal.

In your course and in your upcoming book, you talk about some of the environmental factors that affect our levels of iron. So what are some of those demographics or environmental factors that we might want to think about?

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, you're using more iron. You're often on a calcium rich diet. So high calcium diet is another factor because calcium binds to iron, making you more likely to not absorb iron. There's. Alcohol is a huge contributing environmental factor. If you consume alcohol, then you're going to absorb more iron, but 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, you know, if you eat a high iron diet, you're more likely to absorb more iron. Menstruation, if you're, you know, if you're losing blood through menstruation, that can be a huge amount. You know, that's the equivalent of, you know, potentially donating blood at least once or twice a month or a GI bleed. That's a huge factor. Also, people can use. Lose a lot of blood through a GI bleed. There's, you know, supplements that you take. Some can increase iron absorption, like vitamin C, others can decrease iron absorption. So really, you know, everything that we do has this effect on our iron, more or less. And iron is so important in our health that our immune system really tries to control it. Because even if you get, like an infection that's going to influence your iron levels, your body knows that that iron's kind of like a fertilizer for many infections. And so it's going to, you know, get the iron out of the blood to try to protect you from infection, really being given the fertilizer that it needs.

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?

Yeah, yeah, that's a really important one. So birth control pills, there's a lot of different factors involved in that. One is that estrogen, the estrogen and birth control pills can actually increase iron absorption. But also when you're on a birth control pill, often you're taking it maybe because you have heavy menstrual cycles. And so generally when people take birth control pill, they. A birth control pill, they don't bleed as much as they normally would with like a normal natural menstrual cycle. And so they bleed less, which is a huge factor. You're not losing as much iron. And then in addition to that, a lot of times the placebo pills for like the week off when you're supposed to be menstruating, quote unquote. When you're bleeding on a birth control pill, those often have iron in them. So there's a lot of different factors. And I have seen, like, young girls and teenage girls that develop high iron because they have this hemochromatosis gene, and then they're given birth control and then they. It, like, accelerates the damage. And 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, you know, the pituitary gland and the ovaries.

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. And 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?

Yeah. So you can, you can have all of the above. Everybody's different. I think it's kind of 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 ceruloplasm on blood work, but that's because you're not able to excrete it from your liver like you should be able to. And so it, the copper and the ceruloplasm ends up just kind of 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. So it's hard. We really need to be looking at the genes for those copper diseases and the ceruloplasm and the copper and the red blood cell copper. And then we need to be looking at a full iron panel. And, and this is even something that I struggle with. I'm very comfortable with the iron piece. Now the copper piece is harder because there's, it's, 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. And one of the limiting factors for me is the labs that I love to use. It doesn't automatically include the red blood cell copper and the serum copper and the ceruloplas. And the lab that I love to use, it doesn't even offer the red blood cell copper. So now I'm in a situation where, okay, I'm going to have to order from multiple labs and then I also want a hair analysis on top of that. And I really need, you know, I always look at those iron genes, but I'm having a hard time finding a place to check the copper genes. So 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 and we need to be really careful about just saying, okay, you were low in copper or low in ceruloplasm, which ceruloplasm is a copper dependent enzyme that when you're low in copper, your ceruloplasm can go down. But you can also have that Wilson's disease, where you get low in ceruloplasm because, you know, you're just not excreting it. So we just have to do a better job. And just because you're low doesn't mean that you're actually like low in copper. You could give somebody copper and makes them sick. There is, you know, I hear a lot of people saying, oh, iron deficient anemia. That's a low copper situation. And 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. But I think to just automatically assume that is dangerous.

From a genetic perspective, what are the requirements to be diagnosed with hemochromatosis? You kind of 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.

Yeah, so this is really an important question, and I even have a chapter in my book called the carrier myth. We must end the carrier myth. And basically the carrier myth is this idea that you have to have two hemochromatosis genes to have hereditary hemochromatosis. So there's two hemochromatosis genes that are well documented in the literature. It's, you know, it's. No, not a question as to if they can create high iron. It's been well documented. And the two are what you just said, the HFE C2A 2Y and then the HFE H63. And 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. And that is a really dangerous myth because as I just said, my husband developed hereditary hemochromatosis with just one. And 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. And the reason for that is because that's the most common genotype in the population to have one or the other, like either 1c2a2y or 1h6d3. Now, the more genes you have, the higher your risk. So if you have two instead of one, your risk will be higher, but it is less common to have two than to have one. And really, the way that you diagnose hereditary hemochromatosis is based on labs and genes. So the way you diagnose hemochromatosis, period, is based on blood work. So if you do blood work and you see that somebody has a high iron saturation, high ferritin, you know, 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. And if they have anything out of range, high, or questionable in a functional range, then you need to always get those genes to see, is that what's driving this high iron? And 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. And 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, you know, decades for some people.

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, and that 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 than the H63D and also is involved in lowering hepcidin. So talk to us about hepcidin. What is it? And how do the levels of hepcidin in the body impact our iron levels and our iron storage?

Hepcidin is kind of like 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 breaks on iron. And if you genetically make less of those breaks, then you're going to absorb more iron. And like you said, there is a higher risk with the C2A 2Y because that absorbs more iron. You know, 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 H6D3. Okay, but like I said, there's so many environmental factors, so it's. You know, we can't just look at genes. But, 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. And then that creates just this inability to shut down the absorption. But there's a lot of environmental factors that can infect hepcidin, too. Like, if you have any type of liver disease, that's gonna decrease hepcidin. Alcohol consumption decreases hepcidin, testosterone decreases hepcidin. You know, there's just so many different environmental factors that can really decrease hepcidin, and many of them are pathological, meaning they're not good for you. However, there are environmental factors that can increase hepcidin. So, like, if you get an infection, then that can cause you to have more hepcidin, and that creates anemia of inflammation. So, so 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, you know, pathogens. And so 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. And so basically, what. What happens is you end up increasing ferritin because the immune system saying, put it in the storage unit, get it out of the blood. And so it puts all of the iron into the storage places, and it gets it out of the blood, and then you end up with this massive increase in ferritin that is not necessarily caused by high iron. It's simply caused by, like, inflammation or an infection, which is why ferritin alone is not the best marker for iron. It can also be inflammation.

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. And if we have low iron, that leads to a reduction of hepcidin, which then results in an increased iron level in the blood, correct?

Yes.

Okay, Greg, 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 methylfolate and essentially kind of 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?

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 like, like decrease the expression of the HFE genes. Like I think you're going to kind of 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 chains is kind of of 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. So if we can increase hepcidin and decrease iron, then we can really maybe save some these people from having high iron and iron induced damage.

In your course, you talk about supply and demand for iron. So 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? And 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?

Supply and demand is really a huge part of the story. So the amount of iron that one needs varies and the amount of iron that one consumes and absorbs varies greatly. So people that have the hemochromatosis gene, they can absorb like 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 like 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, but you have to look at, you know, how much blood are they losing? But as far as just like 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 one to three milligrams of iron a day. We lose around one 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 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 in, you know, the United States, there are tons of iron deficient people out there. This is really why the haemochromatosis 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 one to three milligrams a day, that's fine. But if you're like a, you know, if you have a GI bleed or if you're pregnant, you know, you could be losing up to 7-10mg a day, which is huge. And then if you're, if you have the hemochromatosis gene, you could be absorbing 7 to 10 milligrams a day. So my point is there's a lot of different factors and that's why it's so important to look at the labs and the genes and the environmental factors.

So these HFE genes really are a blessing and a curse.

They are, they are. They. You know, historically this gene basically traveled through this Celtic Viking ancestral lineage. And then that's why it's so common in the Caucasian northern European population, especially in Ireland after the potato famine, it got really, really common. But it's traveled throughout the whole world because, you know, globalization, you know, just people travel. So it's not just in Caucasians, that's another myth. But basically, you know, 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, like a warrior survival gene that has been extremely successful. It's just in the wrong environment, which many people now live in, because, you know, our ancestors didn't have a McDonald's on every corner, and they didn't have iron supplements to take, and. And they were iron deficient, anemic, much more than high iron. You know, I just don't think they dealt with a lot of high iron issues because of their environment. Whereas we now have, you know, iron fortified foods and irons everywhere and, you know, sedentary population, which is gonna. The more you're sedentary, the less iron you're gonna lose. There's just a lot of factors that are making this an Achilles heel.

Now, I will admit that I don't even know where the nearest McDonald's is.

But good for you.

So you mentioned earlier that iron can be very oxidative, that it's like rusting from the inside. So are those with lower antioxidant status lower glutathione status? Are they more likely to have negative consequences as a result of the iron overload?

Absolutely. So glutathione is basically like the. One of the anecdotes to oxidative stress. If you. It's like the bulletproof vest to protect you from the free radicals that oxidative stress creates. And so iron, it creates a lot of oxidative stress. Like you watch the Iron Curse in that I cut an apple in half, and one apple, I put, you know, lemon juice on it, and the other apple, I don't. And of course, the apple that has lemon juice is not all brown, and then the apple that doesn't have lemon juice is all brown. And that's oxidative stress. So that's like the electrons are getting stolen from the apple, which is creating a chemical reaction which is causing damage. And 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. And so 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 the. 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 to my husband, honestly, because he, you know, tends to have. He has these genes that cause him to have low glutathione. And I think this is a common situation. And then if you compound that, you know, not just the low glutathione, high iron, but remember what I said about how iron really is bad for the liver because it's, you know, 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.

So let's talk a little bit about some of the testing. You know, 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 basic.

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. So 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, have, you know, either high or low iron, almost, almost everybody. They'll often maybe order like a serum iron or they'll order like a ferritin, but rarely do they order all of them, and you really need all of them. So what's in a full iron panel is the tibc, uibc, serum iron, ferritin and iron saturation. And so the most sensitive markers for high iron are really the ferritin and the iron saturation. And so iron saturation is just looking at a formul of basically looking at serum iron and tibc. So it's important, you know that you're look, you're looking at all this in a fasting state, because if it's not fasting, then your serum iron can go higher. And the truth is your serum iron is kind of like a snapshot it's kind of like a fasting glucose. It can be all over the place. Whereas your hemoglobin A1C changes a little bit slower. So, so the serum iron is kind of like the fasting glucose that just kind of can go up and down depending on how much iron you ate. Whereas the iron saturation and the ferritin, those are gonna more so be likely to reflect kind of like the history, like the long term history of how much iron is really accumulating and building up. And then the TIBC and the uibc. The TIBC is basically looking at how much much transferring do you have to transport iron around the body. And when the tissues are saturated with iron and they're kind of like I'm done, that's enough, stop, then it's going to shut down the, the transferring, which are like the little planes that are flying the iron to and from throughout the body. So when iron's high, the body says no more planes, no more transferring. And then the tibc goes down because it doesn't want to bring any more iron to the tissues. So 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. And it's, it's actually the opposite. So 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 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. So the uib, unsaturated iron binding capacity, like the seats that are open, those go down also. So low uibc, low TIBC happens with high iron, whereas with low iron you'll see more high tibc.

High uibc, 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 is ideal. What are some of the risks of high ferritin? And then where does hein come into the discussion?

If you end up building up enough ferritin, then that ferritin will degrade into hemosiderin. So the body can only store so much ferritin. At some point in time it plateaus and it's like we can get, keep accumulating iron, but we're gonna have to accumulate it as semositerin because Our storage capacity as ferritin is maxed out like it's like a hoarder. Like, we've put the iron everywhere we can in the closets, and now it's just gonna start spilling over out of the closets into the hemosiderin. And hemosiderin is really quite dangerous, not just because it's, it creates a lot of oxidative stress and damage, but it's dangerous because it has an unle unlimited potential to store iron, whereas ferritin plateaus. And, you know, it's not going to be able to store any more iron. Hemosiderin can just keep going forever until it kills you. And, you know, the average person stores around 6 to 10 grams of iron, depending on the person. Somebody with hemochromatosis, they can, they can store as much as 50 grams of iron. So that's, that's exponentially more and that 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, you know, the iron panel or the CBC or those things that are just routine. That's what hemosiderin is. As far as a healthy range for ferritin, you know, 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, you know, 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 summer. And his endocrinologist, I said, just order the iron labs just so that we can see where you are. And he had a high iron saturation, like 56. Iron saturation, high iron, serum iron, but his ferritin was only like 60. Not the most uncommon situation. But 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. And it's. While they try to be scientific, at some point in time, you Kind of 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, you know, that's not a question at all. You know, many people don't get diagnosed till their ferritin's, like, in the thousands. But for managing hemochromatosis, the hematologists really often like to keep it within a very narrow range. Like 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. And 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. If you're showing high iron, especially with the hemochromatosis gene, and you have like a high iron fat and high iron serum, then, then there you still need to be working on supporting lower levels of iron. Cause you have too much iron. That's just, you know, getting to the tissues.

How accurate do we feel blood testing is for looking at this iron picture? And 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.

I think it's fairly accurate. You're right. You know, we don't have an exact idea of what's exactly going on at the cell just because we don't have the lab marker, maybe for that. But I think it's fairly accurate, especially when you start looking at it in combination with the genes. You can really kind of start to assume safely that if somebody has anything that's out of range high with those genes, that, that it's a result of high iron and not result of, like, inflammation, just inflammation. Although inflammation and infection can certainly play a role in that, because like I said, inflammation and an infection, they just drive that ferritin through the roof and can affect the amount of iron in the blood. But 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. And then you need to know, you know, was this just like an anomaly or is this a pattern that's going in the wrong direction just because of high iron?

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?

Most people at this point in time have done 23andMe, and 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, 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. They. If you've seen the 23andMe health reports, then it'll say, you know, 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 like that, that goes back to the carrier myth. You know, my husband and my daughter have the hemochromatosis gene. Their genetic reports say, you know, not at an increased risk because they're misinterpreting the meaning. And that's because of this myth that you have to have two, which is so dangerous.

So 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?

No, anybody can run the genetic detoxification report. They can either go to, you know, Dr. Christy Sutton or genetic detoxification. Either place will get you there. And it's just, you know, $30 for the genetic detoxification report, which has a lot of different genes. And 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. And I need to go back and update the book. Eventually.

You Used the term ferroptosis earlier. This iron induced cellular death. So what are the factors that must be present for ferroptosis to occur and what is it?

Ferroptosis is a programmed cell death that happens whenever you have a lot of iron combined with low free radicals. And what happens is the, the iron creates a lot of damage to the cell membrane. It will damage like the lipid molecules on the cell membrane. And because you don't have enough glutathione and antioxidants to decrease the anti, the free radicals from high iron, then you create so much damage to the cell membrane that the cell basically decides it's going to kill itself instead of create cancer and create more health problems. So the fear optosis itself is a problem because you're, you're destroying what should be healthy tissues. But 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 on low antioxidants, then the ferroptosis will stop. It is a pathological process that is dangerous and creates massive damage to wherever it occurs. But the body does it for a reason. Like the body is trying to preserve itself. It's just sometimes it has to make sacrifices because it's in a bad situation.

You mentioned that iron can affect the brain. So can high iron contribute to, 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?

I think it's very common. Just, you know, from what I've seen and granted I don't have, you know, a couple thousand person double blind placebo trial or you know, meta analysis. Just from what I have seen, I think it's very common. And you know, in the iron curocyte create, 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 haemochromatosis 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 and then that's going to accelerate your risk for neurodegenerative diseases like Alzheimer's, Parkinson's, et cetera.

How about the connection between high iron and blood sugar or even diabetes?

High iron will create damage to the pancreas. Specifically, the beta insulin producing cells of the pancreas are largely damaged. So it can create both type 1 and type 2 diabetes. And then the irony of that, 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.

You snuck in that word irony again.

So if it was a drinking game.

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. So wondering if that toxicant or toxin driving autoimmunity could be something as seemingly benign as iron. And have you seen correlation to autoimmune conditions in your high iron patients? And do those conditions resolve with iron reduction strategies?

There is definitely clinical data that shows that 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. And 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 systems attacking your liver, it's because the liver's damaged largely like 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. And 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. So that's a common issue as far as autoimmune diseases. Autoimmune, thyroiditis, Hashimoto, those as in the literature as well. And 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. But so high iron, I would, I would include that in my autoimmune trigger pro, 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, you know, a chemical or a heavy metal or iron, you know, too much iron is toxic, not enough, that's not good. But too much is toxic. So stress, toxins, infections, gut type issues are big accelerators for autoimmune diseases. Now, the high iron also creates leaky gut, 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 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. And 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 like 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, you know, the immune system is not working as hard, there's less inflammation. But I, I don't think once you've turned those autoimmune genes on from high iron, I don't think that 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.

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 normalize testosterone? And might giving supplemental testosterone in some of these high iron scenarios create more problems?

Definitely. When you talk about testosterone. So testosterone is going to decrease when you have high iron because that iron destroys the testosterone producing cells in the testes and 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. And 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, 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. So it's really dangerous. And the fact that people are testing for and giving testosterone and not routinely testing for iron issues is really kind of disturbing to me. But that's the world we live in, largely is what I find. If somebody has 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 that it's already caused irreversible damage to their testes. And 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. So 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 know, 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 of really serious issues 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. And 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. And 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 a high hemo, 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. It. My colleague's daughter at the age of five was diagnosed with hereditary hemochromatosis. So my point is that these things can happen really early if you have these genes and they're not getting tested for and diagnosed because pediatricians are not running these labs.

Gout is a common condition that we think of as more like an arthritic type presentation as people get older. Is there a connection between high iron and levels of uric acid or gout? And might uric acid also be a blessing and a curse?

High iron definitely causes uric acid to go up, and then when you lower iron, it will lower uric acid. So that's one reason that people with high iron tend to have more gout attacks. But they also get what's called pseudogout, which is where they're 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. And iron's a really bad circumstance that's creating a lot of damage. And so the body creates more uric acid because uric acid is this wonderful antioxidant. And it's just trying to put out the fire of high iron with the uric acid. And then once that fire is put out, because the iron's lowered through whatever mechanism you know, 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.

So can I think then of the uric acid as essentially an antioxidant that is protecting us from the oxidative stress of the high iron levels?

Yes, certainly. Or any other oxidative stress, Whether it's, you know, know, iron or some chemical or whatever. It's. It's protective.

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? And do we want to attempt to increase nitric oxide if our iron levels are still high?

When you have high iron, it will cause endothelial dysfunction, meaning it'll cause low nitric oxide, because it just damages those endothelial cells. And 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. Have that wonderful ability to dilate and, you know, get blood circulating through the arteries. And the capillaries, which is a problem. Having said that, the iron does decrease nitric oxide and I do discuss increasing nitric oxide in the protocols in the iron curse protocols. But I do that at the end of the. It's towards the end. So you've already lowered the iron 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. But I would not recommend one take anything to boost nitric oxide supplement wise until they have lowered their iron and increase their antioxidants. Because if you have high nitric oxide it will react with the free radicals and the 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 what whatnot.

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. So how does iron impact these chronic infections and are the there specific infections that you see more concerning when there are higher iron levels?

Borrelia, like you said, that is manganese dependent, not iron dependent. Yeah, which is interesting.

I didn't know you were an expert on Borrelia, but I'm impressed.

I'm not, but 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. And 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. Now on a case by case basis, like 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 like the literature specifically isolates Borrelia. It doesn't really isolate any other pathogen as far as iron goes. Like 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 and then your immune system's kind of often suppressed just because the high iron can kind of suppress your immune system too. But really more so the issue is it's this breeding ground for high iron. Iron. So 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.

Let's talk a little bit about the hypercoagulation, again, very common in the chronic illness community, those people dealing with Lyme and Babesia mold illness, now long Covid and those types of conditions. So it sounds like iron has an additional impact then on the potential for blood clots or, or hypercoagulation. So in these people that have hypercoagulation, is iron, one of the key things you would be looking at to reduce their hyperviscosity?

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. And that will increase the viscosity of the blood. It's going to make it thicker. So. So, and that's largely because when you have too much iron, the body's trying to find a place to store it. And one place that it will store it is the hemoglobin. And so the body kind of 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 risks for clotting.

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

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. And so they have evolved to create massive amounts of antioxidants. And one of those antioxidants is melatonin. But it's not the melatonin that, you know, you get at night. This is the circulatory melatonin. So the circulatory melatonin is which is made when you go out in infrared light, and that creates massive amounts of melatonin, which creates less oxidative stress stress. So 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 subcellular melatonin. But yeah, any, any antioxidants, whether it's melatonin or glutathione or increasing, know, superoxide dismutase, all of those are going to help decrease mitochondrial dysfunction.

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, and 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.

Once you develop high iron, it's going to basically find your Achilles heel and go after that. So, 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, you know, 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. But 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. But the research, I mean, is pretty clear. It's just about any cancer, whether it's, you know, ovarian, testicular, pancreatic, prostate, blood cancer, bladder. It just, the list goes on. Melanoma skin cancer. So when you create a lot of DNA damage from high iron, creating oxidative stress, your risk for cancer goes up, period.

Now we get to talk about some of the interventions, potential treatment options. So 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.

The first step is lower the iron by removing blood. Okay. And 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 and then they're just going to kind of create another issue. But by removing blood, blood removal is the most common tool used to lower iron and the people that are treated for high iron. And 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 kind of recommendations for people that have hemochromatosis are blood removal as prescribed, avoid, avoid vitamin C supplements, low iron diet, like, avoid red meat and shellfish. That's kind of the big things they recommend. They don't talk about any of the other steps, which I include. So 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. And then the last one is prevention ischemia, reperfusion injuries. And 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, you know, they don't talk about that in the, in the normal allopathic medical world.

So let's dig in just a little bit to each one of these steps. So you were talking about, 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, you know, 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 kind of the way they approach it.

The blood donation rules are changing. It used to be that if a doctor told you to donate blood and you had hemochromatosis, then, then you couldn't just go donate blood. You'd have to maybe, maybe you could go to a blood donation center, but you'd have to like 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, you know, a transmittal infect, transmittable infection, disease. The blood donation piece is, 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, you know, my doctor told me to do this, which is totally kind of asinine. But you know, that's that, 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 in 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. So, so I'm not saying it's not good. It can be wonderful if necessary. But I think just the idea that, you know, anybody can go willy nilly donate blood is kind of misleading. And ideally everybody should get, you know, an iron panel of CBC before they do that.

And 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?

Red meat and shellfish are the highest sources of heme iron, which. Heme iron is much more absorbable than non heme iron. So non heme iron is found in vegetables, fruits. Heme iron is only found found in animal protein, animal products. Non heme iron is found in like the vegetarian vegan type, non animal products. And so this is why people that eat a vegetarian vegan diet are much less likely to have high iron. You know, 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 and in them. And that's why, you know, it's kind of a fallacy for people to believe, like, oh, I'm getting plenty of iron from spinach. Like, oftentimes I'll tell people, well, you're anemic. And they say, well, I eat a lot of spinach. And like, well, you're not. You don't absorb much iron from spinach. It just. It doesn't work very well. Diet plays a role, and if you do have really high iron, then you probably need to be careful about the amount of iron you're consuming until. In your diet, until you get things under control. Control. Personally, I feel like you can eat those foods once your iron's in a normal range if you follow, like, the other steps in the iron curse protocols to, you know, help decrease iron absorption and remove extra iron. But everybody is different.

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?

The most common one that I've kind of used is curcumin, which is an extract from turmeric. And curcumin binds to iron and it removes it. And then there's other ones that bind to iron and remove it, like silymarin and alpha lipoic acid and green tea extract. And all of them kind of have their pluses and minus to them. And I think you kind of have to. To use them specifically, depending on the person and their situation. And then there's other things in the protocols that increase hepcidin, so 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. So the things that increase hepcidin are things like quercetin, berberine, and even melatonin, tonin. And then there's other nutrients that, like the glutathione and the vitamin E and things where that's really just to kind of boost those antioxidants so that you don't have as much damage and fear optosis. And then, you know, there's additional things to help kind of heal up the damage, like phosphatidylcholine and whatnot. And this is where I kind of list a lot of different things on the Iron Curse protocols. And it is. 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.

I had my tablespoon of phosphatidylcholine this morning, so 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 ion equally appropriate.

Surprisingly, there is some research that shows that people that have high iron that take nac, N acetyl cysteine, they actually can create more problems in the short run. And they think that's because the NAC might increase iron absorption. Although I haven't been able to find, like, a real definitive answer on that. That's the hypothesis. And so that is not the case with glutathione. And so for the people that do have high iron, they might want to just do more the glutathione route, the S 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 that kind of helps negate the problems that the NAC can cause. But if you don't know that, you might just give somebody NAC and then that could create more problems.

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?

No. When I said chelate, I was thinking more like curcumin or silymarin or alpha lipoic acid. That's not what they used in the research, but when they do research that compares, like curcumin to prescription chelators, curcumin does just as well, if not better, without the side effects.

Let's talk a little bit about vitamin A and also magnesium in iron regulation. I was a little unclear, clear, because vitamin A is said to increase hepcidin, which would then decrease serum iron. But I've also read that vitamin A can increase the absorption of iron. So when might we want to or not want to supplement vitamin A?

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 ceruloplasm. And so ceruloplasm, like I said, it's this enzyme that needs copper and it actually allows you to get the iron and attach it onto the transfer, the transfer and molecule. So you transport the iron like from the digestive lining to the transfer in via the ceruloplasm. And then once on the transfer in the iron can kind of go throughout the tissues. So when you have low vitamin A, you're not going to have as much ceruloplasm. And then when you don't have as much ceruloplasm, then you can't get the iron. Iron's not gonna be absorbed as well, and then it's not gonna 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.

So I'm, I, it seems somewhat clear now why I was a little confused about the vitamin A.

It's confusing. It really is confusing.

And then how about magnesium? That my understanding is the magnesium can help to minimize some of these iron deposits or deposition of iron in specific organs.

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.

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?

Anybody that's using binders needs to research those specific binders they're using and see, you know, are they binding to iron, are they binding to calcium, you know, 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 were doing a lot of detoxing, they, you know, started getting a lot of side effects from Low minerals, muscle cramps and, you know, not sleeping well and things like that. So I think it's important to do the research on what binders you're taking. I don't have a of lot, a lot of personal experience that I can tell you with specific binders for detoxing, lowering iron, but I think it could happen. I just, I haven't been able to find really good research on like, just in general, some of these binders. How do those affect iron?

Okay.

And I think it's just where you need to check. You need to be checking iron really closely too. But certainly binders can bind minerals and they can bind iron. Iron, which could be good if they have high iron, or it could be bad if they're low.

How often is supplemental zinc or supplemental copper part of your iron curse protocols? And 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?

I tend to use the copper glycinate, which I think is the CU2 too. I've started using copper more within the last year, and I'm certainly using it with people that have high iron because the people that have high iron often will end up with low ceruloplasm. And then if that'll create more issues. Also, if you eat a really high iron diet, that iron's going to potentially compete with the copper absorbent in the first part of the small intestine, and then you're more likely to become low in copper, which can kind of create a vicious problem.

And how about any value of supplemental zinc in these iron curse protocols?

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

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, exercise.

Now that 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. But often many of these people that have hemochromatosis, like they get winded very easily. So you might need a lower iron before you exercise. But exercise stress reduction, trying to really maybe not go to high altitude locations while you are dealing with, 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, sweat daily, get really adequate sleep because when your body's very stressed out, you know, we always need plenty of sleep. But 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, 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 like 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.

So you mentioned sweating. I know people have majored different levels of heavy metals in sweat. In those people doing infra sauna. Do we know if there's any value in infrared sauna in an iron reduction protocol?

I haven't been able to see any research on that, but I do include the infrared sauna and the iron curse. Because you know, if you're getting that near infrared radiation, then you're going to be able to increase more melatonin in the mitochondria and then that extra melatonin in the mitochondria is going to decrease the mitochondrial dysfunction which is a risk of high iron and just in general decrease oxidative stress. So that's that part of it. The other part of it is sweating is going to you, you lose a ever so slight amount of iron and sweat. And so you know, 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 and a sauna.

The last step or step five in your iron first protocol is looking at reperfusion injury injury. Talk to us about what that is and what we might do to avoid additional problems as a result of that.

Reperfusion injuries are not thing. It's not something that's talked about as much as it should be. But when somebody has a stroke or like a heart attack or even if they have like 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, people that end up with liver damage from high iron may need to get an organ transplant. Okay. So when they actually do that surgery. There's often a period of time where there's not enough oxygen going to the liver. Or like, if you're having a stroke, you're not getting enough oxygen to your brain. So that's the ischemia part. The ischemia part is not getting enough oxygen. And then what happens is after the ischemia has occurred, then the body kind of 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. And so the analogy that I use is like the ischemia, the original injury, whether it's the 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 kind of like getting in the car accident. And then the reperfusion injury is kind of like you were, you flew out of the car and you, you know, because maybe you were not buckled up or whatever. So it's like the second injury on top of the first one. And my hope is that people, by doing the iron curse protocols and really kind of honing in on their health, they can be less likely to have these ischemia injuries in the first place, whether it's a stroke, a heart attack, traumatic brain injury, whatever, also be less likely to have that reperfusion injury. And there, so there 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. So it's basically, you know, massive amounts of antioxidants as soon as possible at the moment of the injury.

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. But maybe what people don't always recognize is that there's many types of anemias that are not associated with low iron. So talk to us a little bit about the different types of anemia that listeners should think about.

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. So 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. And then there's anemia from other nutritional deficiencies like from maybe low B vitamins which can be 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. And you know, high iron can cause megaloblastic anemia. It can cause non megaloblastic anemia by causing nutritional deficiencies. It can cause especially the aplastic anemia 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. So 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 then they can re be repopulated. And then you 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 cuz the hepcidin high. So those, those are the major anemias that I cover in the iron curse.

So 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?

Yeah, the ones that I see.

And 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?

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. So pregnant females with the hemochromatosis for 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 are bleeding somewhere. Most likely either a GI bleed or really heavy menstrual cycle or they're like pregnant or something is going on that's really depleting them rapidly. So. But yes, they're less likely to have high iron. Anybody that doesn't have those genes, like myself itself, is at a higher risk for low iron. And then as far as the, that's the hemochromatosis gene part. And you can have hemochromatosis and anemia at the same time. And that would be like a 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 the another type of anemia, megaloblastic anemia.

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?

Iron Ferrous peptinate. 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. And it just kind of is a hard situation. The fact is that any heme iron is going to work so much better. And of course I always like people to get their iron from their diet, but many people do need iron supplements. And whenever I do give iron supplements, I like ferrous peptinate.

So is ferrous peptinate, is that a heme iron?

It's ferrous peptonate that I use is. Yes, it's from animal.

Okay, animal protein. We talked a little bit about vitamin C. So is vitamin C something that potentially would help with iron absorption in those people with low iron? So maybe 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.

This is a hard one because on One hand, vitamin C is this wonderful inexpensive antioxidants accident. 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 the iron, then try to take vitamin C away from the iron foods you're eating or just, you know, get your vitamin C through your diet, which I don't think I would never tell somebody, you know, 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, you know, those antioxidants in the vegetables and fruits. I think you really do need to be careful. You know, people with the hemochromatosis gene might really want to think twice before they supplement with, you know, high doses of vitamin C, a thousand or two thousand milligrams a day, which so many.

People have been doing in the past three years because of the pandemic. Right. So that's something to think about.

I think a lot of the issues we're seeing now, I think it like it's kind of predictable that now everybody, there's this whole group of people that want to talk about copper because like during the pandemic everybody was taking zinc and it's like, okay, well maybe we just made our population copper deficient because you know, everybody was taking zinc and all these things and have we just created these other issues? That's kind of a tangent.

But so you, you, 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 there, is the non heme iron 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, we.

Get benefits from both. The difference is absorption. So absorption happens in the intestines and the heme iron from animal products is better absorbed than the non hemet iron in the fruits and vegetables. So you're not going to be absorbing as much. And, but once you do absorb it, it's all the same. It's just a matter of getting it into your blood.

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. So, for example, Ferrum metallicum or Picana's Feridona or maybe cell salts. Do any of those have a role in trying to increase iron regulation?

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.

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?

So the Iron Curse book will be out in the next couple months, in 2023. And the book mirrors the workshop, educational workshop. Both of those you can find@ironcurse.com of course it'll be available at Amazon, but if you go to ironcurse.com then you'll get some, some other good things there. But 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, you know, five videos and the book, of course, I can go into more depth as far as the research and some of the details.

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. And so 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?

I have Crohn's, so my things are, I have to really spend more of my time and energy focused on my diet than most people because, you know, it's a digestive autoimmune disease. I often, 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 kind of time and energy on that. And then being a working mom that's in the healthcare field, it's, it's not for a lack of knowledge that I don't get, you know, my personal time and do the things that I need to do. It really is sometimes more of like a just time management type issue. And I have relied more and more on kind of having a, a coach to help me, like whether it's a personal trainer or somebody that's an accountability partner to kind of make sure that I'm, you know, getting my workouts in and, you know, doing what I need to do. And my husband's wonderful as far as his sleep hygiene and he helps me with, with that. And then I've also found that I really have to take some days not being in the office to kind of just get my life together. And unfortunately, because I'm in this busy season with promoting the book and getting the book published and everything, I, I've been infringing on my days off more than I'd like to. But I think that's a really important thing and I'm going to claw back and protect those days off for, you know, what life kind of brings up and I need to take care of. And I think that's important. Build in some free time and then, you know, have good relationships with, you know, friends or family or loved ones or whatever. I'm fortunate to have wonderful daughter and husband and good friends. And so those are key.

Wonderful, Wonderful. Such a great discussion. I think you busted a lot of myths. You shared a lot of ironies with us as well. So 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 and just appreciate you and all that that you're doing.

Thank you so much.

To learn more about today's guest, visit drkristy sutton.com that's D R Christy C H R I s t y Sutton s u t t o n.com thanks for listening to today's episode. If you're enjoying the show, please leave a positive rating or review as doing so will help the show reach a broader audience. To follow me on Facebook, Instagram, Twitter or TikTok, you can find me there as BetterHelp. If you'd like to support the show, please visit betterhealthguy.com donate to be added to my newsletter, visit betterhealthguy.com newsletters. This and other shows can be found on YouTube, Apple Podcasts, Google Podcasts, Stitcher, and Spotify.

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