The Iron Elimination Paradox & Weight Loss

I've been reading about Hepcidin, a pro hormone discovered recently in 2000. It is the hormone that regulates Iron absorption and elimination in the body.

There is a lot of evidence via Ray Peat that most degenerative conditions involve excess iron, either directly or indirectly. Hepcidin is produced in great quantities in the presence of inflammation, but while Hepcidin prevents absorption of Iron it conversely prevents the excretion of it also.

So people like myself, with elevated Iron levels and difficulties losing unwanted weight (presenting with other health challenges, not just vanity since excess fat is basically a state of inflammation) may be suffering from a temporary immobilization of Iron, stuck in a paradoxical loop of corrosively high levels of Iron.

I've been taking a lot of B1 (thiamine), as it binds to Iron, and I think it might be helping though I haven't been able to confirm it with a lab test yet, and of course eat a diet rich in inflammation-reducing substances such as saturated fat, fruit, dairy, etc... but as even slight levels of endotoxin greatly exacerbate the inflammation response, it may be necessary for sufferers of Iron excess to have a more targeted and nuanced approach to reducing levels than just giving blood and taking vitamins. I have seen a post that mentioned tetracycline and other antibiotics binding iron (though cows can get it just for being alive, I cannot without an infectious disease get my doctor to give it to me).

Any more insight on this topic would be appreciated.

 

I'm not sure if you can ever be as efficient as blood donation. You could even easily go iron deficient with it, if you did that and a Peat diet that avoids iron fortified foods, so you absolutely need to do blood tests.

 

Apparently Hepcidin sequesters iron away from the blood, so even giving blood in this state can't help as much as it should. Some is contained in Microphages, which would be taken out with giving blood, but most of it is in the liver and fat cells (and probably some other place no one has seen yet). Its almost as if the iron has *disappeared,* but it can't have because it doesn't get excreted from the body.

 

Part of the blood (cells in it) need iron. Iron deficiency would be visible by just looking at those cells, they would appear sick under the microscope. So, wouldn't having that condition be confounded as iron deficiency under some of the blood tests metrics?

 

My hemoglobin, hematocrit, and RBC count used to be elevated above normal, due to high free testosterone (which activates RBC production). After eating a diet consisting of very little iron, mostly consisting of cheese and OJ, for 4 years, and then donating blood 7-8 times in 2-3 years, my iron appears to be depleting. I have donated 3 times since summertime due to my ability to (back home I often couldn't). I donated a couple of weeks after coming to Denver, and to my surprise, the hemoglobin wasn't even higher due to altitude and low O2, but even lower than before, 15 instead of 17. Then it was lower the next time, and even lower the time after that.

So the amount of iron in my tissue is likely very low. My free testosterone is probably much higher than before, yet my RBC count is falling. But, I still don't think supplementing iron is a good idea. I'm not sure if the low iron count is responsible for my morning weakness, but supplementing copper is a much better method to boost RBC, since it not only leads to the creation of RBC, but it also reduces the amount of iron in tissue this way.

Chocolate has tons of both copper and iron, so I highly recommend it if you have low or falling hemoglobin. Unlike oyster, it has saturated fat instead of pufas, doesn't require cooking (BIG plus for me), and it tastes better. Milk chocolate makes life a lot more enjoyable, unlike oysters. Lol.

I don't think the reduced inflammation from low iron will cause weight loss though. Inflammation is caused by so many things, and iron likely has low involvement, if any. I wouldn't focus on weight loss either way. Focus on general health, and you will look good.

 

LOL, are you kidding? Chocolate is nice, but a good oyster soup is heavenly.

 

In the UK at least, as far as I can tell from reading labels, pretty much all "milk" chocolate and quite a lot of dark chocolate would have PUFAs. It seems to be only the darkest chocolate that doesn't.
(I'll double-check some labels next time I'm in a supermarket).

 

Good chocolate will be made with cocoa butter and milk fat if it is milk chocolate, and no other fats/oils. There are cheaper kinds that include other vege oils - I avoid them. Milk and cocoa butter will have some PUFas and MUFAs, but probably OK in moderation, as with butter, cream etc. I think CLA (conjugated linoleic acid) in milk fat is counted as a PUFA, but has some potentially beneficial properties.

 

I agree, but only if oysters were in season all year round. The size and flavor difference is astounding.

@natedawggh
Do you have a source for thiamine binding to iron?

 

I'm gonna find the study but I don't think that's how hepcidin always works, the hepcidin actually traps iron in a good way. Hepcidin shuts iron inside epithelial cells where they die and go to the stool.

The place you don't want iron to get stuck, is the liver and spleen...

Here's the review and the study that suggests that hepcidin causes iron to be passed through the body with the result of iron loss.

http://www.sciencedirect.com/science/article/pii/S1550413105000586
"However, Donovan et al. (2005) propose that intestinal epithelium can take up significant amounts of iron from plasma by transferrin receptor-mediated endocytosis through the basolateral membrane. If circulating hepcidin concentrations are high, basolateral ferroportin is degraded and the iron trapped. At the end of their 1–2 day life span, the iron-loaded intestinal epithelial cells would be shed into the fecal stream. "

Here's a study on hepcidin and hemochromatosis, Expression of hepcidin in hereditary hemochromatosis: evidence for a regulation in response to the serum transferrin saturation and to non-transferrin-bound iron | Blood Journal
"In addition, Nicolas et al demonstrated a severe iron overload in hepcidin-deficient mice and showed that transgenic mice expressing liver hepcidin develop severe iron-deficiency anemia"

A second one, Blunted hepcidin response to oral iron challenge in HFE-related hemochromatosis | Blood Journal

Third: http://www.nature.com/ng/journal/v34/n1/full/ng1150.html