Lowering Iron (chelation) May Stop Alzheimer Disease (AD)

Philomath said:

Why do they always seem to use alpha-tocepherol acetate in these studies? Is it cheaper? More common? If they used a mixed tocepherol would the outcomes be better? As considered through the Peat prism?

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haidut said:

Vitamin E and aspirin are two extremely effective ways of lowering iron levels in both tissues and brain. With that in mind, it is not surprising that both vitamin E and aspirin showed promise in treating Alzheimer's.
Vitamin E may combat functional decline from Alzheimer's disease
http://www.webmd.com/alzheimers/news/20 ... alzheimers
http://www.dailymail.co.uk/news/article ... -pill.html

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NathanK said:

I've been dealing with high iron for years now. My family has a history of high iron and Parkinson's (very northern european thing). I was completely shocked this week when I got my anemia panel back. I started taking Mitolipin 3 weeks earlier and my ferritin halved to 149 from over 300 in the past. Serum iron was cut to 50 (range starts at 45) even though I had an serum iron test done right before starting my new supps and it was 111. My saturation % was considered "low" in the lab ranges at 15% (20% was the cut off). I've taken Vit E before, but did not expect or intend this result. The only other thing I could think that could have assisted in this drop was the DMSO in Melanon and Progestene (I played sparingly with P around the time I started Mitolipin).

I'm not 100% sure if this is great, but it seems like a good thing if I knew what caused this. Maybe the high Vit E content of Mitolipin or possibly the added progesterone (my labs 3 weeks earlier showed my P was at the bottom of the range at .4). Neither aspirin, coffee, or dairy heavy diet has had much of an effect on my iron or ferritin in the past. This was my first ever full iron panel though.

In other related labs, my CRP was .7 (.2 higher than it was 2 years ago, but w/i the 0-1 range) and ESR was at 9 (range of 0-9), which was lower than my pre Peating 28 I had about 3 years ago. My liver enzymes have always been very low (AST @ 17). Whatever I did had some crazy effects.

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haidut said:

Wow, that is a pretty big drop of ferritin. It's probably one of the supplements and maybe it's MitoLipin. The DMSO in MelaNon and Progestene does not have that strong of an iron lowering effect. So, probably the vitamin E in MitoLipin is what's doing this. It would be great if you isolate the effect somehow going forward. I think lower iron is good, provided copper is sufficient. Have you had copper and ceruloplasmin tested?

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NathanK said:

I've been dealing with high iron for years now. My family has a history of high iron and Parkinson's (very northern european thing). I was completely shocked this week when I got my anemia panel back. I started taking Mitolipin 3 weeks earlier and my ferritin halved to 149 from over 300 in the past. Serum iron was cut to 50 (range starts at 45) even though I had an serum iron test done right before starting my new supps and it was 111. My saturation % was considered "low" in the lab ranges at 15% (20% was the cut off). I've taken Vit E before, but did not expect or intend this result. The only other thing I could think that could have assisted in this drop was the DMSO in Melanon and Progestene (I played sparingly with P around the time I started Mitolipin).

I'm not 100% sure if this is great, but it seems like a good thing if I knew what caused this. Maybe the high Vit E content of Mitolipin or possibly the added progesterone (my labs 3 weeks earlier showed my P was at the bottom of the range at .4). Neither aspirin, coffee, or dairy heavy diet has had much of an effect on my iron or ferritin in the past. This was my first ever full iron panel though.

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supernature said:

You present very few iron biomarkers, so its hard to say for certain but i guess indicatively should looks like so:
serum Iron drops from 111 to 50 after 3 weeks on suppl,
TS is 15% after 3 weeks suppl - we could assume it could be 2-3 x higher before start suppl, lets say: 33%
Ferritin is 149, so if we say 2-2.5 x drop after 3 weeks on suppl, it should have been b/w 350-400 before that.
serum Iron after 3 weeks suppl is 50 and your TS is 15%, so TIBC should be 335, which makes UIBC of 285 after 3 weeks suppl.
serum Iron before suppl 111 and TS of around 33% should make TIBC around 330 and UIBC around 220 before suppl.

It seems in just 3 weeks the serum Iron have dropped > 2 x, ferritin dropped > 2 x, TS dropped 2 x, TIBC increased a little and UIBC increased as well.
The unbound-unsaturated iron in transferrin has increased - (i.e. the free and unusable iron thats not bound to transferrin).

This are of course serum values i.e. extracellular, so if they drop, where the extra iron goes if its not taken out of the system via phlebotomy or not present high urine iron elimination.

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NathanK said:

Im guessing i excreted the excess since ferritin is the marker used for intracellular stores when biopsies arent feasible. Haidut posted a paper last year where researchers gathered a rough estimation of liver iron stores by dividing ferritin by AST enzyme lab, iirc. Below 10 was desirable and above 17 was the threshhold for iron overload. The one possibility ive considered is my ferritin was partly high due to some chronic inflammation and the DMSO helped to lower the inflammation. Just another possibility though.

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NathanK said:

This was the first iron panel ive had done. Ive had serum iron and ferritin done every year the past few with little result lowering those values. I need to buy another bottle of mitolipin soon and will have more thorough labs done after that is completed to see more permanence. Though probably not likely, we still cant count out lab error.

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NathanK said:

I've been dealing with high iron for years now. My family has a history of high iron and Parkinson's (very northern european thing). I was completely shocked this week when I got my anemia panel back. I started taking Mitolipin 3 weeks earlier and my ferritin halved to 149 from over 300 in the past. Serum iron was cut to 50 (range starts at 45) even though I had an serum iron test done right before starting my new supps and it was 111. My saturation % was considered "low" in the lab ranges at 15% (20% was the cut off). I've taken Vit E before, but did not expect or intend this result. The only other thing I could think that could have assisted in this drop was the DMSO in Melanon and Progestene (I played sparingly with P around the time I started Mitolipin).

I'm not 100% sure if this is great, but it seems like a good thing if I knew what caused this. Maybe the high Vit E content of Mitolipin or possibly the added progesterone (my labs 3 weeks earlier showed my P was at the bottom of the range at .4). Neither aspirin, coffee, or dairy heavy diet has had much of an effect on my iron or ferritin in the past. This was my first ever full iron panel though.

In other related labs, my CRP was .7 (.2 higher than it was 2 years ago, but w/i the 0-1 range) and ESR was at 9 (range of 0-9), which was lower than my pre Peating 28 I had about 3 years ago. My liver enzymes have always been very low (AST @ 17). Whatever I did had some crazy effects.

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Antonello said:

How much mitolipin were you applying at that time? Also you didn't mentioned if that drop in iron made you feel better or worse.

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haidut said:

Ray has written several times about the dangers of excess iron and its relation to neurodegenerative conditions. He also routinely recommends measuring ferritin and transferrin as more accurate way of assessing iron status.
It seems that some people in Australia exhibit proper cognitive function and propose treating Alzheimer's with iron chelating drugs. Perhaps more importantly, they propose using levels of ferritin as a biomarker predicting Alzheimer's risk and disease progression.

http://www.nature.com/ncomms/2015/15051 ... s7760.html
http://www.sciencealert.com/high-iron-l ... -s-disease

"...Existing drugs that reduce brain iron levels could stop the disease in its tracks. High levels of iron in the brain could increase the risk of developing Alzheimer's disease and hasten the cognitive decline that comes with it, new research suggests. The results of the study, which tracked the brain degeneration of people with Alzheimer's over a seven-year period, suggest it might be possible to halt the disease with drugs that reduce iron levels in the brain. "We think that iron is contributing to the disease progression of Alzheimer's disease," neuroscientist Scott Ayton, from the University of Melbourne in Australia, told Anna Salleh at ABC Science. "This is strong evidence to base a clinical trial on lowering iron content in the brain to see if that would impart a cognitive benefit."
"...At the beginning of the study, the researchers determined the patients' brain iron levels by measuring the amount of ferritin in the cerebrospinal fluid around the brain. Ferritin is a protein that stores and releases iron. The researchers did regular tests and MRI scans to track cognitive decline and changes in the brain over the study period. They found that people with higher levels of ferritin - in all groups - had faster declines in cognitive abilities and accelerated shrinking of the hippocampus. Levels of ferritin were also a linked to a greater likelihood of people with mild cognitive impairment developing Alzheimer's. Their data contained some other interesting takeaways: The researchers found higher levels of ferritin corresponded to earlier ages for diagnoses - roughly three months for every 1 nanogram per millilitre increase. They also found that people with the APOE-e4 gene variant, which is known to be the strongest genetic risk factor for the disease, had the highest levels of iron in their brains."
"..."Lowering CSF ferritin, as might be expected from a drug like deferiprone, could conceivably delay mild cognitive impairment conversion to Alzheimer's disease by as much as three years," the team wrote."


Vitamin E and aspirin are two extremely effective ways of lowering iron levels in both tissues and brain. With that in mind, it is not surprising that both vitamin E and aspirin showed promise in treating Alzheimer's.
Vitamin E may combat functional decline from Alzheimer's disease
http://www.webmd.com/alzheimers/news/20 ... alzheimers
http://www.dailymail.co.uk/news/article ... -pill.html

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NewACC said:

Hello @haidut , I understand that your post is very old and most likely you will not see my message, but still I am very interested in whether you have lost causality in iron research. What I mean is that however reactive free form iron is, it is absolutely indispensable and just infinitely functional. Even mild iron deficiency, which can be VERY EASILY gotten by young people, immersed in the study of Ray Peet's ideas, which abruptly switch to an almost all-dairy diet, along with large doses of aspirin and vitamin E, actually even causes OXIDATIVE STRESS, neurodegeneration, dopamine dysfunction, hypothyroidism, the lack of androgens / progesterone. So why am I talking about this? So maybe the problem is not the level of iron itself, although its excess is clearly TERRIBLY BAD, but a severe deficiency of various "antioxidants", such as excess PUFA, exposure to xenoestrogens / heavy metals, lack of CO2, hypothyroidism, lack of vitamin E, taurine, zinc , copper, vitamin C, lutein, zeaxanthin, various polyphenols, apigenin / naringenin, which would allow iron to do its job without oxidative stress and damage. So perhaps, although iron is the MAIN CAUSE, it would be wiser to maintain adequate iron levels with a just some "antioxidant support" and significant PUFA depletion?

Click to expand...

NewACC said:

Hello @haidut , I understand that your post is very old and most likely you will not see my message, but still I am very interested in whether you have lost causality in iron research. What I mean is that however reactive free form iron is, it is absolutely indispensable and just infinitely functional. Even mild iron deficiency, which can be VERY EASILY gotten by young people, immersed in the study of Ray Peet's ideas, which abruptly switch to an almost all-dairy diet, along with large doses of aspirin and vitamin E, actually even causes OXIDATIVE STRESS, neurodegeneration, dopamine dysfunction, hypothyroidism, the lack of androgens / progesterone. So why am I talking about this? So maybe the problem is not the level of iron itself, although its excess is clearly TERRIBLY BAD, but a severe deficiency of various "antioxidants", such as excess PUFA, exposure to xenoestrogens / heavy metals, lack of CO2, hypothyroidism, lack of vitamin E, taurine, zinc , copper, vitamin C, lutein, zeaxanthin, various polyphenols, apigenin / naringenin, which would allow iron to do its job without oxidative stress and damage. So perhaps, although iron is the MAIN CAUSE, it would be wiser to maintain adequate iron levels with a just some "antioxidant support" and significant PUFA depletion?

Click to expand...