Iron drives heart failure by fattening the heart; iron chelators may prevent/cure

haidut

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Recommending high intake of iron is one of the most common dietary recommendations of registered dieticians, as well as many doctors. The fact that lipofuscin - a highly insoluble complex of iron and PUFA peroxides - increases with age is conveniently ignored in those recommendations. The reality is that iron is a heavy metal and there is plenty of evidence implicating it as a causal factor in infections disease, dementia, Parkinson disease (PD), "autoimmunity", diabetes, CVD, and cancer. The study below now demonstrates that iron, even in physiological concentrations, drives the fattening of the heart after a heart attack, and this ultimately leads to heart failure. Since iron "loves" to interact with PUFA and the latter is preferentially stored in tissues after ingestion, it is likely that most of those fatty acid deposits driving heart failure are made up of PUFA and, consequently, lipofuscin. Conversely, the study claims that iron chelators should be beneficial for both preventing and treating such cases of heart failure. The great news here is that we can go a step further by simply using a natural chemical available in most convenience stores - vitamin E. That humble vitamin is capable of both reducing total body iron stores, as well as preventing/limiting the formation of lipofuscin by reducing the generation of PUFA peroxides (which btw also depend to a great degree on iron availability). In addition, at least one animal study has suggested that vitamin E may be able to dissolve lipofuscin already formed/stored in organs, which further increases the therapeutic potential of this vitamin in heart failure, or aging in general (characterized by increased lipofuscin accumulation). Aspirin is another molecule known to reduce body iron stores, as well as inhibit PUFA peroxidation, though I haven't seen studies on whether aspirin may help remove lipofuscin.

Intramyocardial hemorrhage drives fatty degeneration of infarcted myocardium - Nature Communications
Iron induces chronic heart failure in half of heart attack survivors, according to new study

"...The study, which involved collaborators from institutions in the United States and Canada, followed large animal models over six months. It found that in heart attacks that result in bleeding within the heart muscle—which is about half of them—scar tissue is slowly replaced by fat. Fatty tissue can't push blood from the heart effectively, and this is what leads to heart failure and eventually to death in many survivors of hemorrhagic heart attacks, Dharmakumar said. "Using noninvasive imaging, histology and molecular biology techniques, and various other technologies, we have shown that iron from red blood cells is what drives this process," he explained. "When we removed the iron, we reduced the amount of fat in the heart muscle. This finding establishes a pathway for clinical investigations to remedy or mitigate the effects associated with iron in hemorrhagic myocardial infarction patients." Dharmakumar's team is currently testing iron chelation therapy to do just that in a just-launched clinical trial."
 
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Recommending high intake of iron is one of the most common dietary recommendations of registered dieticians, as well as many doctors. The fact that lipofuscin - a highly insoluble complex of iron and PUFA peroxides - increases with age is conveniently ignored in those recommendations. The reality is that iron is a heavy metal and there is plenty of evidence implicating it as a causal factor in infections disease, dementia, Parkinson disease (PD), "autoimmunity", diabetes, CVD, and cancer. The study below now demonstrates that iron, even in physiological concentrations, drives the fattening of the heart after a heart attack, and this ultimately leads to heart failure. Since iron "loves" to interact with PUFA and the latter is preferentially stored in tissues after ingestion, it is likely that most of those fatty acid deposits driving heart failure are made up of PUFA and, consequently, lipofuscin. Conversely, the study claims that iron chelators should be beneficial for both preventing and treating such cases of heart failure. The great news here is that we can go a step further by simply using a natural chemical available in most convenience stores - vitamin E. That humble vitamin is capable of both reducing total body iron stores, as well as preventing/limiting the formation of lipofuscin by reducing the generation of PUFA peroxides (which btw also depend to a great degree on iron availability). In addition, at least one animal study has suggested that vitamin E may be able to dissolve lipofuscin already formed/stored in organs, which further increases the therapeutic potential of this vitamin in heart failure, or aging in general (characterized by increased lipofuscin accumulation). Aspirin is another molecule known to reduce body iron stores, as well as inhibit PUFA peroxidation, though I haven't seen studies on whether aspirin may help remove lipofuscin.

Intramyocardial hemorrhage drives fatty degeneration of infarcted myocardium - Nature Communications
Iron induces chronic heart failure in half of heart attack survivors, according to new study

"...The study, which involved collaborators from institutions in the United States and Canada, followed large animal models over six months. It found that in heart attacks that result in bleeding within the heart muscle—which is about half of them—scar tissue is slowly replaced by fat. Fatty tissue can't push blood from the heart effectively, and this is what leads to heart failure and eventually to death in many survivors of hemorrhagic heart attacks, Dharmakumar said. "Using noninvasive imaging, histology and molecular biology techniques, and various other technologies, we have shown that iron from red blood cells is what drives this process," he explained. "When we removed the iron, we reduced the amount of fat in the heart muscle. This finding establishes a pathway for clinical investigations to remedy or mitigate the effects associated with iron in hemorrhagic myocardial infarction patients." Dharmakumar's team is currently testing iron chelation therapy to do just that in a just-launched clinical trial."

@haidut Great article and thanks for posting! I have well water that has iron in it. Do you think this might be a factor in someone having too much iron? Would it be beneficial to take extra Vitamin E in this regard?
 

Vanset

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I have been eating 300-400g of beef daily for years and years now and recently tested my ferritin at 179. Recently switched to 97% lean pork. Be careful guys.
 

aniciete

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It's not? I thought it was kinda high, maybe I put more significance to it than needed because the range in my country ends at 230.
Interesting, my range ends at 300. You could probably donate blood and benefit. Apparently with each donation you lose 50-70 points
 

Vanset

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Interesting, my range ends at 300. You could probably donate blood and benefit. Apparently with each donation you lose 50-70 points
Yeah I have not been feeling very well for the past few days. I have tested kinda borderline low in copper as well. I have started taking 2mg of copper glycinate a few days ago, but not feeling anything from it.
 

Dean

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So are the deleterious effects of iron enough to say that you are better off eating white poultry (given what they eat and are fed) than grass-fed beef?
 

tankasnowgod

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I have been eating 300-400g of beef daily for years and years now and recently tested my ferritin at 179. Recently switched to 97% lean pork. Be careful guys.

It's probably not just the beef, but also the lack of bloodletting and intestinal worms and fortified iron you ate (and if you are a male, being male) that got it to that range. Not saying that having intestinal worms is a good thing, but there were lots of ways iron was kept lower in the past, in more primitive cultures, and even in modern ones. Worms weren't really eliminated in most industrialized countries until about the 1960's.

Take a look at the graph below-

iron-intake2.png


So, we have the combination of higher iron intakes (maybe the highest of all time, due to supplements and fortification), along with fewer ways to "lose" iron, with the elimination of things like intestinal worms and being more sedentary and such. It's no shock that ferritin levels (especially in men) are much higher today.

That’s not that high though? Hans has said 50-150 is good.
It depends on the source, and who you believe.

The "lab range" for ferritin is about 30-400. I've heard some suggest it should be more like 30-200.

In the Zacharsky studies, they found a dramatic reduction in heart disease (and cancer, and all cause mortality) when they got ferritin below 90. Personally, I think the target range should be between 25-75, and really, kept at the lower end of that range (maybe like 30-40). There are a lot of studies (by the likes of Zacharsky and Fachinni) that suggest this is a good place to prevent many degenerative diseases. Although I have had ferritin test as low as 18, and didn't notice any negatives. When lowering ferritin from 444 to that near deficiency range (around 30-50), I noticed benefits like improved mood and energy, as well.
 

tankasnowgod

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The reality is that iron is a heavy metal and there is plenty of evidence implicating it as a causal factor in infections disease, dementia, Parkinson disease (PD), "autoimmunity", diabetes, CVD, and cancer. The study below now demonstrates that iron, even in physiological concentrations, drives the fattening of the heart after a heart attack, and this ultimately leads to heart failure.

Remember, Jerome Sullivan came up with the "Iron Hypothesis" of Heart Disease back in 1981.
 
Last edited:

Dannyb

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Recommending high intake of iron is one of the most common dietary recommendations of registered dieticians, as well as many doctors. The fact that lipofuscin - a highly insoluble complex of iron and PUFA peroxides - increases with age is conveniently ignored in those recommendations. The reality is that iron is a heavy metal and there is plenty of evidence implicating it as a causal factor in infections disease, dementia, Parkinson disease (PD), "autoimmunity", diabetes, CVD, and cancer. The study below now demonstrates that iron, even in physiological concentrations, drives the fattening of the heart after a heart attack, and this ultimately leads to heart failure. Since iron "loves" to interact with PUFA and the latter is preferentially stored in tissues after ingestion, it is likely that most of those fatty acid deposits driving heart failure are made up of PUFA and, consequently, lipofuscin. Conversely, the study claims that iron chelators should be beneficial for both preventing and treating such cases of heart failure. The great news here is that we can go a step further by simply using a natural chemical available in most convenience stores - vitamin E. That humble vitamin is capable of both reducing total body iron stores, as well as preventing/limiting the formation of lipofuscin by reducing the generation of PUFA peroxides (which btw also depend to a great degree on iron availability). In addition, at least one animal study has suggested that vitamin E may be able to dissolve lipofuscin already formed/stored in organs, which further increases the therapeutic potential of this vitamin in heart failure, or aging in general (characterized by increased lipofuscin accumulation). Aspirin is another molecule known to reduce body iron stores, as well as inhibit PUFA peroxidation, though I haven't seen studies on whether aspirin may help remove lipofuscin.

Intramyocardial hemorrhage drives fatty degeneration of infarcted myocardium - Nature Communications
Iron induces chronic heart failure in half of heart attack survivors, according to new study

"...The study, which involved collaborators from institutions in the United States and Canada, followed large animal models over six months. It found that in heart attacks that result in bleeding within the heart muscle—which is about half of them—scar tissue is slowly replaced by fat. Fatty tissue can't push blood from the heart effectively, and this is what leads to heart failure and eventually to death in many survivors of hemorrhagic heart attacks, Dharmakumar said. "Using noninvasive imaging, histology and molecular biology techniques, and various other technologies, we have shown that iron from red blood cells is what drives this process," he explained. "When we removed the iron, we reduced the amount of fat in the heart muscle. This finding establishes a pathway for clinical investigations to remedy or mitigate the effects associated with iron in hemorrhagic myocardial infarction patients." Dharmakumar's team is currently testing iron chelation therapy to do just that in a just-launched clinical trial."
@haidut thoughts in someone having really low ferritin though? Just had mine measured at 23! Anything that would raise it outside of liver and red meat?
 

tankasnowgod

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@haidut thoughts in someone having really low ferritin though? Just had mine measured at 23! Anything that would raise it outside of liver and red meat?
While 23 is outside of the lab range (and actually within some lab ranges), I wouldn't say it's "really low." As I mentioned above, mine tested as low as 18. I think many young women frequently test in the teens and low 20s, and young women also happen to be the most resistant to degenerative diseases like cancer and heart disease.

You might also want to get hemoglobin and TSAT checked. Hemoglobin is the most important marker, in terms of anemia symptoms. If you aren't having any anemia symptoms, and hemoglobin is over 12, then you probably don't need to be too concerned about it.

The main things that would lead to ferritin that low would be either blood loss (either mass acute loss, or a more chronic loss), a low iron diet rich in foods with iron blocking compounds (like, say, eating mostly milk and eggs, very low meat), or heavy aspirin use. If any of these apply in your own life, that might be what drives the lower number.
 

Apple

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AlaskaJono

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So, we have the combination of higher iron intakes (maybe the highest of all time, due to supplements and fortification), along with fewer ways to "lose" iron, with the elimination of things like intestinal worms and being more sedentary and such. It's no shock that ferritin levels (especially in men) are much higher today.
Yes, I read a study 20+ years ago regarding the 'lowered risk' of heart attacks in Men who gave blood yearly, or had jobs where serious cuts occured throughout the year ( ie- blood loss). The main idea was that because women (until menopause) lose blood regularly (monthly) through menses, then their overall heart attack risk was less than men.
(So Boyz....let's get out there and bleed?! - oh wait, that doesn't make Somebody any money....) If I trusted the medical industry I would give blood now, save a few bags for myself if I get injured, and the rest to the hospital, but.... no way José now, in this day and age of genetic data collection/selling.
 

DrJ

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I recently found out I have hereditary hemochromatosis. My ferritin was close to 400 but people who don't catch this condition earlier can be in the thousands. My iron saturation was over 60% which is very high. Thanks to everyone posting these things.

It's pretty common in North European people (like 1 in 150) so worth getting tested for if you have high iron and fit the ethnicity. Leeches might have been legit lol
 

tankasnowgod

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A ridiculous study that doesn't really test the hypothesis. As I mentioned above, the Zacharski studies found that Ferritin needed to be under 90 to have heart attack prevention benefits. Even though those studies found benefits, the Zacharski studies didn't even hit their target ferritin levels, as they were aiming for a near deficiency level near 25. The above quoted study used a cutoff of 350, grouping people into "above" and "below." Plenty of men in the "below" 350 could be well above 90, and certainly above the ferritin levels found in pre-menopausal women, which tend to be in the 20-50 range.

This is a poorly conducted study that does nothing to refute the iron hypothesis.
This article (not a study) from 2002 also does nothing to refute the Iron Hypothesis. In fact, it doesn't even claim to, simply saying that there is "not enough evidence at the time to support the hypothesis." Zacharski had already published a small, very positive study in 2000, but the longer study (also with impressive results) wasn't published until 2007. Fachinni was also publishing some of his impressive iron reduction studies in the same year, 2002, so there is lot's of great evidence that we have access to now that Christopher Sempos didn't have when he wrote that article. That article was also published two year's prior to E.D. Weinberg's book "Exposing The Hidden Danger of Iron."
Dr. Jerome L. Sullivan, III, the pathologist who first theorized of a link between heart disease and iron levels in the blood, died Friday, May 3, 2013, of complications from diabetes. He was 68...
So what? Sullivan's untimely death does nothing to invalidate his hypothesis, especially seeing as heart disease wasn't the cause of death. I'm guessing that Sullivan suffered from Type 1 Diabetes, as iron reduction is known to reduce (or even "cure") the impaired glucose utilization seen in Type 2 Diabetes. In fact, high iron may even be the primary cause.

And if you want to play the anecdotal evidence game, I would counter with Iron Researcher E.D. Weinberg and his wife, both who employed iron reduction strategies (he used aspirin and calcium channel blockers, his wife donated blood). He died just after his 97th birthday, and was survived by his wife, who was 91 at the time-

 

oxphoser

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Yeah I have not been feeling very well for the past few days. I have tested kinda borderline low in copper as well. I have started taking 2mg of copper glycinate a few days ago, but not feeling anything from it.
Why not just eat some copper containing foods on a weekly basis, such as beef liver, shitake mushrooms or squid (which is cheap!)?
 

Vinny

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A ridiculous study that doesn't really test the hypothesis. As I mentioned above, the Zacharski studies found that Ferritin needed to be under 90 to have heart attack prevention benefits. Even though those studies found benefits, the Zacharski studies didn't even hit their target ferritin levels, as they were aiming for a near deficiency level near 25. The above quoted study used a cutoff of 350, grouping people into "above" and "below." Plenty of men in the "below" 350 could be well above 90, and certainly above the ferritin levels found in pre-menopausal women, which tend to be in the 20-50 range.

This is a poorly conducted study that does nothing to refute the iron hypothesis.

This article (not a study) from 2002 also does nothing to refute the Iron Hypothesis. In fact, it doesn't even claim to, simply saying that there is "not enough evidence at the time to support the hypothesis." Zacharski had already published a small, very positive study in 2000, but the longer study (also with impressive results) wasn't published until 2007. Fachinni was also publishing some of his impressive iron reduction studies in the same year, 2002, so there is lot's of great evidence that we have access to now that Christopher Sempos didn't have when he wrote that article. That article was also published two year's prior to E.D. Weinberg's book "Exposing The Hidden Danger of Iron."

So what? Sullivan's untimely death does nothing to invalidate his hypothesis, especially seeing as heart disease wasn't the cause of death. I'm guessing that Sullivan suffered from Type 1 Diabetes, as iron reduction is known to reduce (or even "cure") the impaired glucose utilization seen in Type 2 Diabetes. In fact, high iron may even be the primary cause.

And if you want to play the anecdotal evidence game, I would counter with Iron Researcher E.D. Weinberg and his wife, both who employed iron reduction strategies (he used aspirin and calcium channel blockers, his wife donated blood). He died just after his 97th birthday, and was survived by his wife, who was 91 at the time-

So, aspirin reduces iron, right?
 

miraddo

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Yes there is much evidence that aspirin lowers body iron stores through a couple of mechanisms:
1) mucosal blood loss. Even a daily loss of 1 ml of blood might substantially alter iron stores over time.
2) direct chelation of free iron

So, aspirin reduces iron, right?
 

Vanset

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Why not just eat some copper containing foods on a weekly basis, such as beef liver, shitake mushrooms or squid (which is cheap!)?
Beef liver too high in vitamin a for me. Squid I have no access to and sea food is kinda sketchy. Mushrooms? Maybe. I might try them out.
 

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