Hemochromatosis and Autoimmune Conditions

I was reading a paper which says it can indicate a functional iron overload, instead of a genetically predisposed iron overload. As per my memory, I am heterzygous for HFE, meaning that I carry a risk but that the risk is relatively minor.

Anyone got any ideas?

Or maybe stuff that you have done to improve your health results in mixed results. The saturation looks pretty high though. You could donate blood a couple of times and then see if there are any changes.
 
Or maybe stuff that you have done to improve your health results in mixed results. The saturation looks pretty high though. You could donate blood a couple of times and then see if there are any changes.
I know,

Whats even stranger is that the saturation has increased a lot since adding back in vegetables and some carbs.

Here are my results from July, when I had been pretty hardcore carnivore for around a year, including organ meats:

1577795523353.png

The only thing which was out was the TIBC. So since then things have definitely gotten worse - so I am guessing I am not "hemochromatotic", but it is a functional thing.


The waiting list for donating blood is like three months here, so I am thinking of just blood letting myself to hopefully bring it down.


One thing I did read was that GGT is a relatively marker for glutathione depletion and oxidative stress in the liver as a consequence of iron storage overload. My GGT was excellent, but my cells don't seem to want any more iron... that seems for sure :huh:
 
Hi,
I would like to share result of using IP6 (Inositol Hexaphosphate) for 2 weeks.
My last blood check done 03.03.2021 showed 48% saturation of blood transferrin.
Check done yesterday 01.04.2021 showed 33% saturation of blood transferrin.

Two things I was doing during this time were:
1. using IP6 500mg total 20 capsules during last month
2. autohemotherapy - 7 shots 11ml - some blood was escaping also

What comes to my mind as possible additional influence on result of staturation of blood transferin is that Iron as well could have been "used" by foreign organisms like:
- bacteria (I was sick for one week shortly after first blood test in the beginning of March) and spiting some greenish stuff from my nostrils and sinuses
- parasites (about that I do not know if I have) or
- tumor (about that I do not know if I have).
- or that iron was packed to some tissues

And just to add that I do not have hemochromatosis (checked by genetic test).
 
My last blood check done 03.03.2021 showed 48% saturation of blood transferrin.
Check done yesterday 01.04.2021 showed 33% saturation of blood transferrin.

Two things I was doing during this time were:
1. using IP6 500mg total 20 capsules during last month
It's good to know, specially for those who can't do bloodletting!
 
The below is a great interview between Dr. Mercola and his guest, Morley Robbins.

Morley talks about the 4 types of Iron, and something that (it is indicated) most doctors don't realize, is that they know that 70% of iron is carried in the blood, so decanting makes sense to make less if need be, but the problem is that is what is in the cells, which copper regulates. And what iron that is in the cells gets deposited in the liver and spleen - difficult to remove, which again is where copper comes in.

 
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I know,

Whats even stranger is that the saturation has increased a lot since adding back in vegetables and some carbs.

Here are my results from July, when I had been pretty hardcore carnivore for around a year, including organ meats:

View attachment 32970

The only thing which was out was the TIBC. So since then things have definitely gotten worse - so I am guessing I am not "hemochromatotic", but it is a functional thing.


The waiting list for donating blood is like three months here, so I am thinking of just blood letting myself to hopefully bring it down.


One thing I did read was that GGT is a relatively marker for glutathione depletion and oxidative stress in the liver as a consequence of iron storage overload. My GGT was excellent, but my cells don't seem to want any more iron... that seems for sure :huh:
I really couldn’t find the place to put this but a quick search of the forum didn’t turn up anything on iron supplements or how it’s absorbed in the body. The short answer is that the body uses heme or ferrous iron for the most part, which is the Fe+2 ion, and doesn’t use the ferric or Fe+3 ion. There’s lots of things that can inhibit iron absorption which are well known to the forum but listed in the article.

The reason I was looking this up had to do with food preservation and generally if you cook meat to a well done state, you change the iron inside from the needed ferrous +2 state to the +3 state which isn’t optimal for absorption. That means the old ways of food preservation like charcuterie might be superior by preserving nutritional value.

The article about how cooking changes iron and other nutrients in meats.

 
I've had great success with using IP6 with inositol to reduce my iron load. Unfortunately I can only donate blood in the UK every 12 weeks, so letting wasn't really an option.

I've posted some screenshots below. I took the manufacturers recommended dose of this each morning for around two months then recently got retested. Now I'm just taking a scoop once a week and will get checked again in a few months. The first reduction after my tests a few years ago was also due to using IP6, but less intensely.

The biggest improvement I noticed was being able to gain weight and not have sore muscles for 5 days after a workout. If anyone struggles with getting access to blood letting the IP6 supplement may be a good alternative. 👍
 

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I've had great success
Hello Jono, I'm very interested with your mention of IP6 with Inositol and your great results. I've never heard of it apart what I've read on Google just now and when I last had blood tests my iron reading was very high.

I cannot give blood as they said my veins were too small so this would fit the bill, maybe. Which one did you use. ?...I clicked on your detail but nothing comes up.
 
Vitamin D controls the metabolism of iron:

Hepcidin

In 2001, a small antimicrobial peptide produced in the liver was identified and called hepcidin (from hep- “liver”, and -cidin from “microbicidal”). Hepcidin is cationic, amphipathic, and rich in cysteines, which generate four intramolecular disulfide bonds and stabilize the molecule in a folding structure β. Hepcidin is active against Gram-positive bacteria, but also inhibits the development of some fungi and Gram-negative bacteria with an antibacterial spectrum similar to that of β1-defensin. Nemeth et al. showed hepcidin production in response to interleukin-6. Other inflammatory cytokines also induced its synthesis, but to a lesser extent. Hepcidin is the main regulator of iron homeostasis, because it binds to ferroportin, the only known iron transporter to the outside of the cell. Hepcidin binding to ferroportin induces the internalization and degradation of ferroportin, which blocks the exit of iron from the cells. The cells mainly affected by this interaction include enterocytes (which block iron absorption in the bowel) and macrophages (which prevent iron release into blood). The consequence is the occurrence of the so-called “anemia of chronic diseases”, due to decreased circulating iron concentrations. Low serum iron levels restrict iron availability to extracellular bacteria, which are deprived of an essential nutrient and are therefore easier to kill. Paradoxically, however, intracellular pathogens (Salmonella, Mycobacteria, Candida, etc.) have greater amounts of iron available and may thus more easily develop inside macrophages, which therefore increase the local production of hepcidin to kill the germs.

Calcitriol has also been shown to modulate the iron–hepcidin–ferroportin axis. Bachetta et al. showed that the calcitriol-VDR complex may directly inhibit hepcidin expression by binding to a VDRE at the hepcidin promoter. On the other hand, calcitriol decreases interleukin-6 production in response to the lipopolysaccharide, and thus indirectly decreases IL-6 secretion. In healthy subjects and patients with kidney failure, it has been shown that when 25-OH vitamin D levels increase, hepcidin decreases and anemia improves. Interestingly, a Spanish group had already shown that the intravenous administration of calcitriol to patients on hemodialysis improves anemia and reduces the need for erythropoietin.


The antibacterial protein hepcidin regulates the absorption, tissue distribution, and extracellular concentration of iron by suppressing ferroportin-mediated export of cellular iron. In CKD, elevated hepcidin and vitamin D deficiency are associated with anemia. Therefore, we explored a possible role for vitamin D in iron homeostasis. Treatment of cultured hepatocytes or monocytes with prohormone 25-hydroxyvitamin D or active 1,25-dihydroxyvitamin D decreased expression of hepcidin mRNA by 0.5-fold, contrasting the stimulatory effect of 25-hydroxyvitamin D or 1,25-dihydroxyvitamin D on related antibacterial proteins such as cathelicidin. Promoter-reporter and chromatin immunoprecipitation analyses indicated that direct transcriptional suppression of hepcidin gene (HAMP) expression mediated by 1,25-dihydroxyvitamin D binding to the vitamin D receptor caused the decrease in hepcidin mRNA levels. Suppression of HAMP expression was associated with a concomitant increase in expression of the cellular target for hepcidin, ferroportin protein, and decreased expression of the intracellular iron marker ferritin. In a pilot study with healthy volunteers, supplementation with a single oral dose of vitamin D (100,000 IU vitamin D2) increased serum levels of 25D-hydroxyvitamin D from 27±2 ng/ml before supplementation to 44±3 ng/ml after supplementation (P<0.001). This response was associated with a 34% decrease in circulating levels of hepcidin within 24 hours of vitamin D supplementation (P<0.05). These data show that vitamin D is a potent regulator of the hepcidin-ferroportin axis in humans and highlight a potential new strategy for the management of anemia in patients with low vitamin D and/or CKD.

 
Hepcidin is very low in the third trimester of pregnancy, which is a period when the women have the highest level of estrogen. And estrogen is involved in iron metabolism. And also activates vitamin D, which decreases hepcidin.

Serum hepcidin levels substantially decreased from 19.39 ng/mL in the first trimester to 1.32 ng/mL in the third trimester.


Hepcidin concentration decreased gradually from the first to the second and third trimester to undetectable levels (≤ 0.5 nmol/L)

 
I was looking at some studies about high altitude and iron metabolism, and there was one thing that came to my attention. In this study, they had two groups that they sent to high altitude environment. Prior to that, one group was infused with iron. And in that group, the hepcidin remained high for 48 hours. They think that transferrin was a cause of that because it also fell after 48 hours. Ferritin remained high for 144 hours, so it played no role.

Taken together, these findings demonstrate that the suppression of hepcidin by hypoxia is too fast to be generated by a reduction in iron availability, suggesting that erythropoiesis and/or hypoxia per se are the major physiologic regulators in this setting. Iron loading can overcome the suppression of hepcidin by hypoxia during the period for which transferrin saturation remains elevated, but not during the entire period for which ferritin remains elevated. This finding is consistent with the notion that transferrin saturation is the major signal linking iron availability to hepcidin up-regulation, but intrahepatic iron has also been reported to enhance hepcidin expression directly. The latter phenomenon could explain the slightly higher hepcidin levels after 48 hours in the iron-loaded group, compared with the saline group, despite similar transferrin saturations.

What this could mean in practice is that, if you plan to improve your red blood cells by going to high altitude, you should not consume iron rich food, such as meat, during that time period. You can load yourself with iron before you go, but not during the high altitude period. Or, if you plan to stay there longer, you can cycle.

Or, if you are a premenopausal woman, you could avoid eating meat during the days when your estrogen is high.
 
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