Season 5, Episode 5: Iron Overload and Hemochromatosis with Dr. Christy Sutton – Part 1

Evelyne: I have wanted to do a show on hemochromatosis since the idea of this podcast first came up. And if you listen to our episode with Dr. Mark Houston, which aired in January, 2024, I mentioned then that I have a heterozygous mutation for hemochromatosis. So there will be more personal stories from my end than usual. And because there’s so much to talk about, this episode will be split into two parts.

I am really excited to learn more about hemochromatosis because as I was going through Christy’s book, The Iron Curse, I was reminded how important this information is and I just don’t see it talked about very much in our field. So about our guest. Dr. Christy Sutton is a chiropractor who’s interested in asking why health problems happen and finding the safest and least problematic solutions. Getting to the root of the problem is the foundation of her writing, teaching, and clinical practice. She takes a deep but meaningful dive into genomics, lab testing, and creating a personalized health plan. Her focus on finding and avoiding health landmines early stems from her personal experience with Crohn’s and celiac disease, plus her husband’s experience with high iron and a pituitary tumor. Christy, before we kick off, what is lighting you up this week?

Dr. Christy Sutton: So what is lighting me up right now is I get to watch my daughter play on an all-boys soccer team this weekend for the first time. Because she’s always played with girls, and now it’s all boys because there’s no girls in her grade that want to play soccer.

Evelyne: Oh, wow. Well, that’s fun.

Dr. Christy Sutton: It’ll be fun to watch her.

Evelyne: That’s amazing. Thank you for sharing. So Christy, we are about all things hemochromatosis and iron overload today. First of all, I’d love to know how did you get into this topic and really diving so deep into it that you wrote a book about it, and not just a little book, a very lengthy, very thorough book called The Iron Curse.

Dr. Christy Sutton: Yeah, it was definitely more thorough than I intended, but I think it’s better than I intended, I think. But so what led me into writing this book is helping my husband get diagnosed with hereditary hemochromatosis. He was dealing with liver issues and he was also having some gastric issues, but he had some elevated liver enzymes and it wasn’t being properly diagnosed as hereditary hemochromatosis. And I had seen his labs, which his doctor was ordering, and they were being dismissed and not really addressed and would tell him, “You need to donate blood.” And he would donate blood periodically. But it wasn’t until I was writing my first book that I wrote a book before the Iron Curse called Genetic Testing: Defining Your Path to a Personalized Health Plan. And that book goes through a laundry list of genes, a lot of different genes and what they mean, what you can do about it, the epigenetic genetic stuff.

And I wrote a part about the hemochromatosis genes, which honestly I didn’t know very much about those genes at all, but it was a part of my kind of research into genetics back in, I don’t know, 2017. And then I realized, “Oh, this gene exists. I understand what it means now. It means you’re more likely to get high iron.” And my husband had that gene, which explained why I kept telling him, “You need to donate blood.” And why the high iron was causing his liver to be inflamed and have problems. So we walked him through the process of him getting properly diagnosed. Which, that was much more difficult than it should have been. I think you have a pretty clinical audience, so I can go into those clinical details.

Evelyne: We would love that.

Dr. Christy Sutton: Okay. Because most people would be like, “I’m bored now.” But I can go into it with you all. Okay. So basically what happened was we went to the gastroenterologist, which, a gastroenterologist, it is within their scope of practice to diagnose and treat hemochromatosis. And my husband was having liver issues, GI issues. So we went there and I gave the gastroenterologist the labs that both my husband’s doctor and I had ordered extra on my husband. And I gave my husband’s doctor the genes and the gastroenterologist took it all in. And then I think he basically dismissed it. And he went and did his lab work and evaluation and all of the imaging. And that process misdiagnosed my husband as having autoimmune hepatitis. So they had a false positive for autoimmune hepatitis come back. And so he had… That test is a smooth muscle antibody test. If you have a positive smooth muscle antibody, that’s a test for autoimmune hepatitis.

And so they said, “Okay, you have autoimmune hepatitis. Take this drug for a year, that’ll fix it. And basically come back in a year and your liver will be better and everything will be better and you’ll be better.” And that didn’t ring true to me, what I understood about autoimmune diseases, because I have Crohn’s and celiac. So I understand this is a lifetime of management, not just a year of drugs. But my husband who has a very different mindset than me, not in the healthcare field, was like, “Cool, I’m going to take that option. Just give me the medicine for a year and I’ll be better.” And so I didn’t have a lot of faith in them. So what I did was he started taking the medicine for the autoimmune hepatitis and I rechecked the labs. And the labs showed that he did not have the smooth muscle antibodies, but his liver enzymes were getting worse along with his iron-related labs were getting worse.

And then the gastroenterologist said, “Okay, you know what? You just have mild fatty liver, you need to lose some weight and go to the hematologist because I think you have polycythemia vera.” Which, the reason he thought my husband had polycythemia vera is because polycythemia vera causes high red blood cells just genetically. And so the solution is to remove blood. My husband did have high red blood cells, he had high hemoglobin, he had high hematocrit, he had high iron, high ferritin, high iron saturation. He had all of the hemochromatosis labs that were showing up to be a problem. But so we went to the hematologist, the hematologist, immediately I gave him the labs and genes and he was like, “Hereditary hemochromatosis. Easy, no problem. Everything’s going to get better once we fix this. His liver is going to get better, his testosterone is going to get higher.” Because he had low testosterone. Because hemochromatosis causes low testosterone, “He’ll probably lose weight. His stress hormones will come down.”

Because periodically my husband had high stress hormones. So then everything did get better except for my husband didn’t lose weight and his DHEA did not come down. So then we went to the endocrinologist, and at this point in time, I have learned that my husband does not know how to give a medical history. Because I’ve been sitting in doctor’s appointments with him, watching him and watching the doctors ask him questions. And I realized my husband cannot give a medical history and the doctors are not asking the right question to get the information out of my husband. So what I did was I let my husband meet the endocrinologist, give his spiel to the endocrinologist, say everything he wanted to say, and then I basically came in after that and said, “And here’s what you need to know.”

And then I told everything that I had observed and seen and I summarized it with, “And I think he has Cushing’s disease.” Which is where you have high cortisol. And she said, “No, he doesn’t have Cushing’s. He doesn’t look like somebody with Cushing’s because typically people with Cushing’s, like they have a very swollen face and they’re really overweight. A lot of the weights in their belly.” My husband was swollen for himself, but he just looked like somebody that drank too much beer, even though he didn’t drink beer at all. So he said, the endocrinologist said, “His blood sugar’s normal. He doesn’t look like somebody with Cushing’s. It’s not Cushing’s.” I get it. She was probably just trying to calm my worries. But then about six to nine months later, my husband’s getting the first of two brain surgeries to remove the pituitary tumor that was causing Cushing’s disease.

So why is this important in this part of the story? Because hemochromatosis, high iron deposits throughout the body. And one of the places that it likes to deposit is the pituitary gland, specifically the anterior pituitary gland. So I believe that my husband, had he been properly screened for at a young age for the hemochromatosis genes and properly diagnosed at a young age and monitored and not allowed to have high levels of iron and high levels of oxidative stress, and probably made some better lifestyle choices in his 20s, would not have developed that pituitary tumor, which created the Cushing’s issue that we had to deal with and have dealt with for so long. So that’s the high iron piece. Why did I write a book about high iron? That started it. Then I went back to my office… I know I’ve been talking for a long time, I just have a little bit more to say and then you can interject. Sorry.

Evelyne: This is great. No, I absolutely loved that story, and I think it’s so common with so many people, especially with hemochromatosis to… Or that it’s never looked for. That it’s quote, unquote, “Not a big deal.” And that it can take so long, just like it does with a lot of diseases, right? Where you have to go see multiple doctors and it keeps being missed. So please continue. I think it is a great and fascinating story.

Dr. Christy Sutton: Yeah. So then I go back to my practice. So I’m all along during this period of time, I’m still seeing patients and I’ll often either look at the patient’s labs that they bring in from their other doctor or order labs to try to figure out what’s going on here. And I would also want to look at the genes. So a lot of people that did 23andme, I would look at their genes and they sequence some of the hemochromatosis genes.

And what I realized was that a lot of people have hemochromatosis. And they were not getting properly diagnosed. And that was disturbing to me. What was more disturbing to me is… Keep in mind, I’m a chiropractor, so it’s within my scope to diagnose this, but I cannot treat hemochromatosis. So I have to refer out for treatment. So what was more disturbing was that I would refer people out to treatment, and often they would go to their primary care or they’d get a second opinion from a cardiologist or whatever, or they’d try to get in with a hematologist and it would be next to impossible because it’s hard to get in with a hematologist unless you have cancer.

So they were dismissed and they were basically told, “You’re fine, don’t worry about it.” Many times. Over and over and over. And that to me was so frustrating. And then on top of that, my colleague’s daughter developed hereditary hemochromatosis when she was five. And that is a whole rabbit hole that we’ll have to go down at some point in time. I talk about it in the book. But that was a serious… I was like, “I have got to write a book about this.”

Evelyne: Wow.

Dr. Christy Sutton: So that’s why I had to write about the high iron. Now, personally me, I’ve struggled with low iron almost my whole life for many reasons that are complicated. So I could not write a book about iron and not put some pieces about low iron in there.

Evelyne: Absolutely. Wow. Thank you again for sharing that story. So fascinating. With hemochromatosis, is it synonymous with iron overload? What is the actual definition of hemochromatosis?

Dr. Christy Sutton: So hemochromatosis is synonymous with iron overload. Really the distinction is if somebody has a hemochromatosis gene and then they have hereditary hemochromatosis, you don’t typically want to call somebody that has hereditary hemochromatosis iron overload. Typically… You can, and it means the same thing. It’s just hereditary hemochromatosis generally is not called iron overload. Non-hereditary hemochromatosis, people that just have high iron because maybe they’re eating a lot of red meat or maybe they have well water that has a lot of iron in it, or maybe they’re just taking iron supplements when they shouldn’t be, people that don’t have the hemochromatosis genes and develop hemochromatosis, that can be called iron overload.

But if you have a hemochromatosis gene and you develop hemochromatosis, which we can talk about exactly what that means on labs to develop hemochromatosis, but if you have a hemochromatosis gene and you develop hemochromatosis, then that is hereditary hemochromatosis. If you’re in the UK, they call it genetic hemochromatosis. It’s all the same thing. But yeah, the UK has a lot of hereditary hemochromatosis because the gene is very prolific in Caucasians, especially in the United Kingdom.

Evelyne: Yeah, I want to talk more about that. And I do have a clarifying question. So is it only hereditary hemochromatosis if you’re homozygous for the SNPs or heterozygous as well?

Dr. Christy Sutton: Oh, that’s a good question. I’ll tell you the actual truth and then I’ll tell you the myth. The truth is that if you have one hemochromatosis gene and you develop hemochromatosis, you have hereditary hemochromatosis. Period. There is a myth, I call it the carrier myth. And the carrier myth is that if you have one hemochromatosis gene, then you’re safe from hemochromatosis, and you have to have two hemochromatosis genes to have hemochromatosis. And this is basically totally misusing the word carrier. Which is confusing a lot of people out there, and clinicians, and the education has got to get clear on this. Because this one fact could help so many people get screened for better and diagnosed. Because right now there’s a lot of people that are being told, “You only have one gene. You’re fine. Don’t worry about it. You have to have two.” And that is a dangerous myth.

The truth is that if you have one hemochromatosis gene, you will absorb iron better than somebody without a hemochromatosis gene. And then the question is, do you absorb iron to the point where it becomes pathological? And you can do that with one hemochromatosis gene. It just depends on your environmental circumstances. You can have two hemochromatosis genes and not develop hemochromatosis because you have all of these factors that are going to make you low in iron.

Like maybe you got a gastric bypass and you’re not absorbing iron, but you have two hemochromatosis genes. Or maybe you just have malabsorption issues because you have celiac and you’re not absorbing anything. Maybe you have a GI bleed, maybe you have horrible menstrual bleeding. Maybe you are on a vegan diet, maybe you just take a bunch of supplements that make you low in iron. There’s so many different factors. The genes do not give the diagnosis. The diagnosis is given based on the lab work. The genes just tell you is it hereditary and this is going to be something you have to manage and watch closely for the rest of your life, or is this non-hereditary and this will likely be an isolated incident as long as we get to the bottom of what’s going on and get the iron levels lower.

Evelyne: Got you. Thank you. You mentioned that it is more common in the UK. I was born and raised in Belgium, and so I think that’s probably why I am a carrier. So how common is it in the US?

Dr. Christy Sutton: So there’s a good study that I reference in the Iron Curse. And that study looks at… They looked at 10,000 people and they basically looked at the genotype, homozygous and heterozygous for two out of three of the hemochromatosis genes. So C282Y and H63D. And then they looked at the people that have one of those genes or heterozygous, and then they looked at people that have compound heterozygotes. So they have one of the C282Y, and one of the H63D. So one of the two main ones. That’s a good study. They didn’t look at the third hemochromatosis gene, the S65C. But they did look at the two main ones. And they looked at it, and basically about 30% of the American population has a hemochromatosis gene. So this is extremely common, especially in Caucasians, just not commonly diagnosed.

People that have hemochromatosis, it tends to take 10 years and three doctors before they get the diagnosis. And the people that do get diagnosed, it’s only 2 out of 10 people actually get diagnosed. So most people are not getting diagnosed. The few people that are getting diagnosed, it takes 10 years on average, and many people it’ll take decades, but most people, they just don’t get diagnosed. Maybe they die of a heart attack and nobody knows they actually died of a heart attack because they had high iron. So the reason that they’re so… Being in Belgium, you are definitely in the hemochromatosis hotspot. The highest percentage is in Ireland. Because the United Kingdom… Basically this gene originated in a likely Viking ancestor thousands of years ago. And it was clearly a successful, helpful gene to have, because it has… And it makes sense because so many people have died of low iron throughout the ages from just not getting enough iron-rich foods or having a wound or menstruation or childbirth.

And so this gene really helped people survive to and through childbirth, and it was very successful, but it started in a Viking. Those Vikings clearly landed in the United Kingdom, and then they also landed throughout Europe and traveled throughout Europe. I mean, the gene is basically everywhere now. Not really that much in Asia, but Northern European, big time. And then of course what happened in Ireland was they had the great famine, and I learned you don’t want to call that a famine because the people in Ireland do not call it a famine. They call it a genocide. I got in big trouble with a bunch of Irish people on TikTok for that. But basically they call it a genocide because while their potatoes did die, the queen basically took away a lot of their food to take it to England. And so they call it a genocide because they would’ve had food enough to survive through this period of time without potatoes due to the potato blight.

But they instead died. Over a million people died in Ireland because the food was taken away. They couldn’t fish in their waters. The other crops that they had grown were taken away from them. Their other poultry, all the food, it was all taken away. And so over a million people died during that and a couple other million moved away, a lot of them to America, which is why we have so much hemochromatosis genes here.

And so the reason I’m saying that is because the reason Ireland has the highest percentage of hemochromatosis genes is because it was already there in a large percent of the population, because that Viking ancestor was already there. And then they’re on an island, so they’re kind of inbreeding. And then they have this genetic bottleneck where the people who have the hemochromatosis gene survive the famine, genocide, whatever you want to call it, the period of time with no food. And at the other end of that famine period of time with no food, there is a explosion of hemochromatosis in Ireland because now the people who had the gene survived and they all had kids that have two genes, which makes it more likely to get hemochromatosis.

Evelyne: Fascinating. Wow. I was actually going to ask you what would’ve been the genetic advantage at some point with the body absorbing too much iron? So super fascinating because it’s not advantageous to us anymore now.

Dr. Christy Sutton: I think it is.

Evelyne: Tell me more.

Dr. Christy Sutton: Well, because I see… I had come from it from the perspective of somebody that’s been struggling with low iron for a long time, and I come also from the perspective of seeing a lot of patients that struggle with low iron. And I think it is advantageous, especially if you have one hemochromatosis gene, which most people do. Because if you have one hemochromatosis gene, you are going to be less likely to be low in iron. It’s almost like the Goldilocks principle. It’s like you’re less likely to get too low, you can still go too high, but it’s less likely to happen especially during the period of your life where you’re childbearing. Because the main reason that women lose blood is because they’re menstruating or pregnant, which are two huge iron-losing events that we have to deal with. And so really the way evolution works is the mechanism of action for evolution is childbirth.

And so the hemochromatosis gene gets you up to and through delivering that child because you’re less likely to die of low iron. And then what happens after childbirth is not as relevant. While it’s important to make sure that child can grow up and have more children, it’s not as relevant because you can’t have any kids when you’re 50 years old anyways, as a female. Your childbearing years are over. So if you now have heart disease and Alzheimer’s and Parkinson’s and liver failure because of high iron, evolution doesn’t really have a say in that and doesn’t care about it. So I think it is advantageous, but it’s a double-edged sword. That’s why if you know have the gene or genes and you watch your iron levels closely, it doesn’t have to be a problem at all. It’s only a problem if you’re unaware and not being monitored, and the iron levels are allowed to go high long enough to cause permanent damage.

Evelyne: I have some clarifying questions on the genes that you mentioned. So you mentioned the C282Y. Is that the RS number of the HFE gene? And then I thought that when you say you have two copies of the gene or one copy of the gene, I thought it was, if I’m heterozygous, I have one SNP in that gene. Am I misunderstanding the terminology?

Dr. Christy Sutton: Yeah. Okay. So the C282Y is like HFE C282Y. So HFE is the hemochromatosis gene. And then the SNP, the single nucleotide polymorphism, that is C282Y, is the RS number… And I can’t remember the RS number right off my head, but I can look it up if you want me to. So that is the RS number. Okay. So there’s three hemochromatosis genes and they all have different RS numbers. And you… So the HFE, H63D has a different RS number, and then the HFE S65C has a different RS number. And basically they’re all SNPs within the hemochromatosis gene. And so that one gene you will inherit one from one parent and one from the other. So of those three, you can only inherit two copies from that group of three. It just depends on which one your parents have. So my parents didn’t have any hemochromatosis genes, so I don’t have one. But your parent gave you one bad one and then one normal one.

Evelyne: Right.

Dr. Christy Sutton: So you can have a C282Y and a H63D and be a compound heterozygote. You can have a C282Y and a C282Y homozygous, and that’s the worst possible option because you absorb the most iron with that combination. But you can only inherit one copy from your mom or your dad. So those are the options, either normal or one of the three variants that increase iron absorption.

Evelyne: Okay. And like you were saying in the beginning, some of the genetic testing tests for all three, though it’s less common, but if I’m not mistaken the… Is it the H63D, that’s more… That’s the most common of all of them to inherit?

Dr. Christy Sutton: Yeah.

Evelyne: Okay.

Dr. Christy Sutton: H63D is the most heterozygous… Heterozygous H63D is the most common. The truth is there’s not a lot of data on what I call the third gene, the S65C. So of the data that I’ve looked at, the H63D is the most common. Heterozygous for that is the most common. And then, and that might come down to the Goldilocks principle too. That’s the one that you absorb more iron, but not quite as much as the more problematic C282Y.

Evelyne: Got you. Very interesting. Thank you for clarifying that. So I have some questions about some of the symptoms and dangers of iron overload both acutely and over time. So can you go into that? And your book is actually, the whole title is The Iron Curse: Is Your Doctor Letting High Iron Destroy Your Health? So it’s some pretty strong language. So what are some of these dangers of the iron curse?

Dr. Christy Sutton: Well, iron likes to… The body doesn’t have a really great mechanism for losing or removing iron. You lose a little bit, but not a meaningful amount just as a healthy person. So assuming you’re not losing a lot of iron because of blood loss or something pathological iron will accumulate, the body likes it, very much needs it. And has over time really developed ways to save it for a rainy day and kind of hoard iron for when you need it later. And so the iron likes to accumulate largely in the liver. That’s one of the first places that it likes to accumulate as ferritin and hemosiderin. And so wherever the iron accumulates, it will cause damage, it’ll cause oxidative stress. So it might first start in the liver. What does that look like for the liver? Liver cancer, 200 times increased risk for liver cancer. Liver inflammation, fatty liver, decreased bile production, just overall liver issues. Decreased ability to detoxify because of liver problems.

Okay, so that’s the liver. Where are other places that iron likes to accumulate? Iron also likes to accumulate in the heart. So what does that look like? It will cause cardiovascular disease because you’re going to be getting a lot of oxidative stress, so you’re going to get more plaquing of the arteries. You’re going to be more likely to have a stroke and a clot. Because not only is the iron accumulating, but people that have hemochromatosis tend to have thicker blood because they tend to have more red blood cells, more hemoglobin, more hematocrit. They have thicker blood and that means that they’re more likely to clot. If you have thick blood with a lot of oxidative stress from high iron, then you’re going to have clotting. You’re going to have… Iron like to accumulate in the pancreas causing type one and type two diabetes. People that have hemochromatosis are often called bronze diabetics because the iron will accumulate in the skin and cause the skin to make more melanocytes creating this kind of weird bronzing.

And if you have this bronzing of the skin with diabetes, that’s a common hemochromatosis pattern. Iron likes to accumulate in the anterior pituitary gland. So what does the anterior pituitary gland do? It makes hormones. So it makes hormones that will… Like ACTH, which will affect your cortisol levels. It makes LH and FSH, which will affect your testosterone and estrogen and progesterone levels. So you get lots of issues with infertility, low testosterone, hormonal problems, period. Anterior pituitary gland makes TSH. So you’re going to get more issues with thyroid. You might have an increase risk not just for Hashimoto’s thyroiditis, but also just regular old hypothyroidism. It makes growth-stimulating hormone, the anterior pituitary gland. So people with hemochromatosis, if they have hemochromatosis at a young age, they are more likely to have stunted growth. Not always, but more likely to have stunted growth because their pituitary gland is not making the growth hormone like they should.

High iron likes to accumulate in your gonads, your ovaries and testes. What does that look like? Infertility, low sperm count, low egg quality, low sperm motility. So iron likes to accumulate in the joints. Well, what happens is your body basically has more inflammation and makes more joint inflammation, and so you get more joint pain. That’s really common for people with hemochromatosis to have a lot of joint pain. So I mean, iron likes to accumulate in the brain. What does that look like? Well, the basal ganglia is particularly at risk for high iron levels. So what does that look like? Parkinson’s disease. Iron likes to accumulate in the hippocampus too, and the rest of the brain, what does that look like? Alzheimer’s disease, bipolar, depression. These are all clinical findings of hemochromatosis. Iron likes to accumulate everywhere and it likes to accumulate in your digestive lining causing leaky gut, digestive issues, increased risk for autoimmune diseases. Really mitochondrial dysfunction.

I mean, the list is very… This is where… It’s truly an iceberg disease. The tip of the iceberg is maybe just joint pain, fatigue, maybe some high liver enzymes. But if you go under the surface, there is very few health problems that hemachromatosis doesn’t increase the risk for. Infections. Iron is like a fertilizer for infections. For almost every pathological infection will get worse if you throw iron into the equation, with the exception of a few. Like Lyme disease doesn’t care for… Lyme Borrelia doesn’t care for iron, it likes manganese. But pretty much everything else likes iron. And if you have high iron, your immune system is going to have a harder time getting rid of infections, which is why the immune system takes the iron out of your blood whenever you do have an infection. So that’s something else we could talk about as far as labs and what that can look like and the role of how that works in the body.

But so yes, the short and long answer is yes. I have some strong language on my cover of my book and there’s a reason for it. I mean, we’re talking about a disease health, iron disorder, that is easy to screen for, diagnose, and treat. Most people are not getting screened, diagnosed, or treated, and it is costing this country, and not just this country, but a lot of other countries, a lot of money and unnecessary bills for treating diabetes and heart disease and joint pain and all of these things that are just symptoms of the underlying problem. And this is so easy to treat and prevent and we’re just not even looking for it. And we’re totally misunderstanding it. So yes.

Evelyne: Christy, this is all truly frightening and we will talk about solutions and we will also dive into labs. What I think is interesting too about this is that men usually develop symptoms between, I think it’s like 40 to 60 and women after menopause. And so by then, if they are undiagnosed, so much damage has already been done at that point. And I think that’s truly one of the scary parts as well.

Dr. Christy Sutton: Certainly one of the problems is that even if you do get diagnosed and treated and you get into the managed range where your iron levels are now in a healthy range, you still have a lot of iron that’s been stored in your body from having undiagnosed hemochromatosis for a long time. So the sooner… Ideally we don’t have this situation where you go high, you shouldn’t have to go high, but if you do go high, it needs to be fixed early and addressed early so that you don’t have all this extra storage of iron because it can take a long time to get all that iron out of storage and to heal up the damage. And at some point in time… This is one reason that there’s an increased risk of not just liver cancer, but pretty much every cancer with hemachromatosis. You just get more DNA damage because of all the oxidative stress.

So it is a problem. And yes, women are more likely to get hemachromatosis when they’re postmenopausal, but I think we need to be careful about categorizing people into this over-50 crowd. Because while women and men are more likely to get hemachromatosis the older they get… For men, it’s just they’ve had more time to accumulate iron over time. And women, they become postmenopausal and now they basically are accumulating iron rather than losing it. But we need to be careful about saying it’s more the over-50 crowd. I think when we categorize things like the over-50 crowd is being the highest risk, I think that means we’re going to miss a lot of other people that have this problem like children or men and women that are in their teens, 20s, 30s, 40s. And so I think what we need to do is we need to just say everybody needs to have a full iron panel workup every single year.

And I think everybody, at least in America, should, and many other parts of the world should be screened for the hemachromatosis genes.

Evelyne: Absolutely.

Dr. Christy Sutton: And I say everybody, not just Caucasians, because I see a lot of non-Caucasians in America that have the hemachromatosis gene because Europeans colonized the Americas. And so when they colonized the Americas, they brought their genes with them. My receptionist from Honduras has a hemachromatosis gene and a celiac gene, which also is very common in Ireland and the European countries. And I see it in people that are not Caucasian, but they have the gene. So I think in America, this gene is really here. We just need to be screening for it and dealing with it. Europe, they need to do the same as far as I’m concerned.

Evelyne: Agreed, agreed. I feel like this is a good time to tell you a little bit more about my personal story with it and the diagnosis aspect, and then we’ll get into what that looks like and what are all the labs we should be looking at. So you really had me diving down some of my own rabbit holes of lab work and PubMed when I was preparing for the show, but so my symptoms initially were fatigue. Some of the same symptoms as low iron. And as I’m telling this story, you’ll understand why I’m also just so passionate about this. So as I was researching, I came across some emails from 2011. Yes, I still have them in my email museum. And my dad at the time was working for a pharmaceutical company and one of his colleagues was a nephrologist at UCSF who then connected me with this iron specialist in New York.

And I ended up finding some of his papers on iron, both anemia and overload, Dr. Gary Brittenham. And he referred me to Dr. Gordon McLaren, who’s at UC Irvine. And then he was the one who recommended the hemochromatosis test, which is how I found out that I was a carrier. Interestingly, I mentioned his name to Dr. Gordon McLaren, because he’s been involved in an ongoing study called the HEIRS study, which stands for Hemochromatosis and Iron Overload Screening study, looking at the prevalence across different races in the US and Canada. And it looked like the last time they published was in 2020, but they had looked at 62,000 people at that point. I think they were trying to enroll a 100,000. So that was interesting. But anyway, I had emails, or I in that email chain I had lab results going back to 2005, 2007. And at that point, I already did have a history of having high iron levels, high iron saturation, though not necessarily high ferritin.

And I remember when I was in college, I think it was my third or fourth year, and I had Kaiser insurance at the time, and I remember this conversation quite vividly because I spoke with the lead hematologist of Kaiser here in San Diego because I was concerned about my high iron levels. And I wanted to speak to somebody. And he told me that it wasn’t something to worry about until you’re in menopause. And I said to him, “You’re telling me there’s nothing I can do until I’m older?” I just didn’t believe that. And now I don’t remember exactly what I did or didn’t do after, and obviously I don’t take multivitamins with iron, but I wish that I had managed it better over time. And because of my inability to donate blood for many years, and the reason is that it wasn’t until the fall of 2022 that the FDA lifted the ban on donating blood if you lived in certain countries in Europe, like I did in Belgium in the ’80s and ’90s, because of mad cow disease, in case you had acquired it.

And so I lived in Belgium till 1997. And so because I was in my 20s at the time, I didn’t want to pay to have therapeutic phlebotomies done, and my Kaiser doctor didn’t want to recommend it. So at various points in the last 15 years or so, it has normalized at times. It has gone really high at times. I’ve also had B12 deficiency anemia. So I’ve had anemia symptoms at various points while having high iron, but also having normal ferritin most of the time. So I find that very confusing and I want to dive deeper into those.

So can you tell me, with the diagnosis of iron overload, what are the markers that you are looking at? And I just want to remind the listener that we do have full transcripts of each show available on our website at podcast.designsforhealth.com. So if you’re listening in the car right now or you’re on a walk and you want to take notes on all the labs, it’s all there. And I also wanted to mention that Christie’s book is the most comprehensive resource on all things iron that I’ve seen, including all the lab values and so much more. And this is not an ad. Obviously Christie didn’t ask me to say this. I just found it to be such an amazing comprehensive resource. So let’s talk about the labs.

Dr. Christy Sutton: Thank you.

Evelyne: Yeah.

Dr. Christy Sutton: Yeah. Labs are really the meat and potatoes of the diagnosis. So the technical diagnosis, we first need to start with what are the labs that diagnose hemochromatosis? And there’s basically two things you have to have to check the box of hemochromatosis. You have to have an iron saturation over 45% and a high iron. Now, there’s two problems with that. One problem is that most labs allow iron saturation to go over 45% before they flag it as high.

And that’s just… I don’t know why the labs do that, but I know that the technical hemochromatosis threshold is 45% for iron saturation. And that has to be with a ferritin that is “high”, quote, unquote. So what is a high ferritin? Because that’s a big question. Because the lab ranges for ferritin in my opinion, allow people to go too high and they vary from lab to lab and from man to female. And me personally, I don’t ever like ferritin to be over 100. And that is much lower or somewhat lower than most labs. A lot of labs will allow females to go to 150 before it’s high for ferritin or males to go to 350 or 400 before they’re high for ferritin. And those are much too high. Period.

If you have a hemachromatosis gene, then it’s often recommended to stay in the range below 75 on ferritin. Just so you don’t go too high. You have basically 50 to 75. Some doctors even want you below 50 on ferritin. I know my husband, his doctor wanted him below 50 for a period of time to really get the liver enzymes down as fast as possible. So there is some research that I cite in the book that really supports my idea of not going over 100 on ferritin. There was a study that looked at the chances of surviving COVID and getting long COVID, and the chances were higher, you were more likely to die of COVID or get long COVID if you had a ferritin over 100. They narrowed it down to 20 to a 100 for ferritin. I don’t like 20. I think 20 is too low.

I really think more like 50 to 75 is a really healthy range, if you want to have a healthy range. I know that’s narrow, but that’s kind of the target goal that I have in general. Most people. So there is another study that I reference in the book, and I even have an image of the ferritin, the chart of the ferritin, as people… There’s a direct correlation between your ferritin getting higher and your life getting longer. So people that have hemochromatosis are more likely to have a shorter life for many reasons. But what this research says is that they looked at ferritin above and below 200. They didn’t break it down to a 100, they started at 200. I wish they’d started at a 100. But they started at 200 and then they went to 300 and 400 and 500 and 600, and they graphed the increased risk of dying compared to ferritin. And it’s a direct correlation.

The higher your ferritin, the shorter your life as far as the averages go. To the point where if you’re over 600 on ferritin, that can take decades off of your life. So when people want to talk about longevity and they’re not talking about hemochromatosis and ferritin, I just think that’s such a missed opportunity. Why do we have to talk about doing an ice plunge when we’re not even diagnosing the hemachromatosis?

Evelyne: Yeah.

Dr. Christy Sutton: Let’s get to the meat and potatoes of the problem and then we can talk about microtuning our mitochondria.

Evelyne: Excellent point. Yeah.

Dr. Christy Sutton: So those are the two big labs, the ferritin and the iron saturation. Now, okay, everybody needs to be getting a full iron panel every year. And what’s included on the iron panel is a ferritin, a serum iron, a TIBC, a UIBC, and iron saturation. Okay? And then you really need to always get a CBC with that, because people that have hemochromatosis often will have abnormal findings on the CBC. They might have high red blood cells or high hemoglobin or high hematocrit. They could also have low red blood cells. You just don’t know, but you need that CBC because the CBC tells you if they can have blood removed. If you have low hemoglobin or you have low red blood cells, you are not a good candidate for having blood removed to lower iron because you have anemia. If you don’t have enough healthy red blood cells or hemoglobin, you’re anemic. Okay? So you can have too much iron and be anemic.

It’s called iron loading anemia. So the CBC tells us, do you need… Can you remove blood? And the iron panel tells us do you need to remove blood? Or do you need to work on lowering iron? It really tells you, do you need to work on lowering iron, are you too high, are you too low? The labs in the iron panel like the TIBC, that is looking at basically how much transferrin… So iron needs a chaperone. And the chaperone for iron is transferrin. Because the body knows it needs iron, but it also knows iron is kind of a problematic mischievous child that needs a chaperone. Because if iron is just, let’s say, injected into your veins, you get an iron infusion, then it will go throughout the body and create oxidative stress. Because iron will go and react with whatever it can react with and create lots of damage and rust the body basically.

This is why a lot of people that get iron infusions have these horrible reactions. So when you eat iron, then you absorb it. And through the process of your absorption, the body attaches it to transferrin, and when it gets attached to transferrin, then it’s in the blood and it hops on transferrin. And the transferrin is like an airplane that flies the iron throughout the body, wherever it needs to go, and then takes it, and then the iron gets off the transferrin airplane and goes into the cell. And that’s a whole another part of the story. So the TIBC is basically looking at how many transferrins are available for iron to hop onto and fly around the blood. And if you have too much iron, then your body’s like saying, “No more iron. Get rid of the airplanes. The airport is full, no more incoming planes.”

And then the transferrin goes down and the TIBC goes down. So when you have too much iron, the TIBC goes down. And when you don’t have enough iron, the body’s like, “Hey, we need more iron. Send us more iron.” And then the TIBC goes up because the body makes more transferrin for iron to hop onto and take iron throughout the body. This is why when women are pregnant and they’re really working hard to make a human being, their TIBC goes up often. Because they need so much iron that their body’s like, “More transferrin, more transferrin, get us more iron, get us more iron.” That’s also because those women are also anemic. They need more iron. They’re iron deficient anemic at that point in time. Okay, so that’s TIBC. Now, UIBC is… TIBC always needs to be… Iron panels always need to be done fasting so that you have a baseline apples to apples. Because they can change depending on what you ate a couple hours before.

So UIBC is basically the unsaturated iron binding capacity, and that’s saying, “How many open seats do I have on these planes that are flying iron around my blood?” And if you have a lot of iron and hemochromatosis, then all of those seats, all of those seats are taken on the plane. So there is no unsaturated transferrin. They’re all saturated with iron. So it’s all saturated, there’s no unsaturated transferrin. And then the unsaturated iron binding capacity, also known as the UIBC will get low as well. The opposite side of the story is if you have low iron, then your body’s going to have a high UIBC. Why is this important? Because I see that often one of the first things that happens when people are dealing with a high iron situation is their TIBC or their UIBC will get low while everything else is within a quote-unquote, “normal range”.

And I have lots of feelings about what normal means. And I think I talked about some of that with the iron saturation and ferritin, but it’s important for two reasons. We need to understand that TIBC and UIBC get low when you’re high in iron and high when you’re low in iron. Because a lot of people, they get confused and they’re like, “Oh, I’m not too high in iron. My iron levels are low on labs.” It’s like, “No, your TIBC and UIBC are low.” Or… They go low when you’re high and they go high when you’re low in iron. Okay? So that’s important to know.

And so if you have the TIBC and the UIBC, then you have the serum iron. And the serum iron will… That’s just analogous to a fasting glucose. So the serum iron is basically just how much iron is in your blood at that moment in time. And all of these labs can hop around very quickly depending on if you’re sick. This is another reason we need to look at the CBC to see, are you sick? Do you have high white blood cells or neutrophils or lymphocytes or whatever? Because if you’re sick, then what happens is the body, the immune system knows iron is like fertilizer, and it’ll push the iron out of the blood and it’ll store it. It’ll basically, it’ll increase hepcidin. So we can talk more about hepcidin. But hepcidin is like the control mechanism for iron absorption. And then when you increase hepcidin, the iron absorption drops down and you get less iron in the blood, but the ferritin goes up.

So this is where you get a high ferritin and a low iron, and that’s like anemia of inflammation. So whenever you’re inflamed because you’re sick or whatever, you’re just inflamed, then often what will happen is the ferritin will go up because you’re taking the iron out of blood to put it into storage temporarily. So the ferritin pops up. This is why ferritin is also an inflammatory marker. And often the serum iron will go down. I mean, you can go back and recheck the labs 1 to 14 days later, and they can be dramatically different just depending on your health and how it changes. So yeah, that’s the iron labs in a nutshell, I guess.

Evelyne: This wraps up the first part of our interview. Make sure you tune in for the second part of our conversation about iron overload and hemochromatosis, where we’ll dive into strategies for optimizing protein intake while also being careful with red meat intake. We’ll talk about the link between high iron and low copper, and we’ll also get into key supplements for reducing iron. We’ll talk more about genetic testing insights along with many more clinical pearls on hemochromatosis, but also on anemia. So make sure you tune in next week for the continuation of this conversation.

Voiceover: This is Conversations for Health with Evelyne Lambrecht, dedicated to engaging discussions with industry experts exploring evidence-based cutting-edge research and practical tips.