86 replies to this topic

[lucid]

I can't for the life of me imagine how self-selection of being a blood donor could account for an 86% decreased risk of heart failure.

Yeh I couldn't imagine that it would be all from self-selection, nice find on that study. It would be nice if this topic got some media attention, would save lots of healthcare money and would also put a permanent end to blood shortages

[bgwowk]

So, there you have it.

...an "association", not a proof of causation.

[Shepard]

It would be nice if this topic got some media attention, would save lots of healthcare money and would also put a permanent end to blood shortages

Doubt it.

[lucid]

Doubt it.

Hmm, which part?

[Shepard]

About ending blood shortages. Mostly due to general apathy among the population.

[bgwowk]

I think it's likely that blood donation is healthy, but definitive proof isn't available.

The more general question is, "What is the optimum amount of iron (by what assay?) for long-term health?" There is circumstantial evidence that being a bit below the population average may be good, just as is true for weight, blood pressure, etc. Although I must say that the correlation between low iron and cognitive deficits that someone pointed out is a real shocker. You had better be sure low iron is good for you, because the price of living longer by this mechanism may be decreased intelligence. And that in itself is kind of scary given the known associations between lower intelligence and degenerative brain disease.

[eternaltraveler]

And that in itself is kind of scary given the known associations between lower intelligence and degenerative brain disease

How big of an association is this? Could it be that someone with higher intelligence simply has farther to fall before they are classified as having a regenerative brain disease?

[bgwowk]

Don't know. Don't know if anybody does.

[lucid]

"What is the optimum amount of iron (by what assay?) for long-term health?"

I would like to know that too. Given pre-menopausal women have lower mortality rates for various diseases, I think until someone shows me a study showing the optimum iron levels, I am going to give blood once a year mimicking blood lost via menstruation so long as my blood iron content isn't too low. I guess I could also get my blood iron checked every 4 months, then give blood if it is above some optimum level (who knows what that is..?). I will probably just do the once a year thing.

[xanadu]

Lets get back to iron chelation. Is there any reliable way to do it and what is the best way? I'd rather not bleed, there has to be a better method than that!

[stephen_b]

So, there you have it.

...an "association", not a proof of causation.

I wasn't implying proof of causation with my comment.

The only way to disprove the assertion that blood donations reduce heart disease fatality would be to have a truly random pool of test subjects. Not quite sure how to do that. But is the pool of subjects that researchers get by putting an add in the paper any less self-selective?

I suspect that the real issue is scientists, like other people, are unwilling to consider an idea they know can't be right.

Stephen

[bgwowk]

Lets get back to iron chelation. Is there any reliable way to do it and what is the best way? I'd rather not bleed, there has to be a better method than that!

Iron chelators are administered intravenously, and only bind free iron, so I'm not sure how much good they would do for someone who doesn't have toxic iron overload.

If you want less iron, donate blood or eat less of it. As I said earlier in the thread, running will cause iron loss too. The question remains, how much iron deficiency, and by what measure?

[shifter]

Us Imminists that donate blood probably help our recipients extra from all the goodies we take

[Mind]

For some recent research presented at UABBA, check here.

Iron may increase muscle wasting late in life.

In rats, the scientists found pockets of excess iron in muscle cell mitochondria, the tiny power plants found in every cell. The excess iron affects the chemistry inside the mitochondria, sparking the formation of harmful free radicals that can lead a mitochondrion straight to the emergency exit, said Christiaan Leeuwenburgh, Ph.D., a UF professor of aging in the UF College of Medicine and the Institute on Aging. Leeuwenburgh was the senior author of the study and of a related report published online this month in Aging Cell that details the damage done by excess iron in mitochondria.

"We become less efficient at an old age and we need to understand why this is," Leeuwenburgh said. "One thing, maybe, is the accumulation of redox-active metals in cells. If the mitochondria become unhappy or are ready to kick the bucket, they have proteins in the inner and outer membranes that they can open up and commit suicide. They're tricky beasts."

The suicidal mitochondria can damage the rest of the muscle cell, leading to cell death and perhaps to muscle wasting, a big problem for adults as they reach their mid-70s, Leeuwenburgh added.

At UABBA Leeuwenburgh claimed non-heme iron was the big culprit when it comes to cellular malfunction.

When I started this topic, I was unsure about iron. Now I definitely side with the lower than average argument for longevity (for men) - based on research in the last year or so - and if I am getting iron, it would be nice to have only heme iron.

[david ellis]

Donating blood is an effective way to get rid of stored iron (ferritin). Aug 06 I had a ferritin level of 132 with a reference range of 22-322(ng/mL). By May 07, my ferritin was down to 55. Donating three units of blood did it.

When I did this I was only aware of the post-heart attack/stroke risk. The infusion of high ferritin level blood causes most of the damage post attack. I was pleased to read the research in this post and discover that my health was benefited even without a dramatic event.

It certainly makes sense that ferritin will cause damage without a dramatic event, ferrritin iron is highly reactive when released. Early mammals had to defend their iron supply against against bugs, leeches, tapeworms and bacteria. Ferritin evolved as a safe storage of very reactive iron. Modern man doesn't need this storage system as much because modern life has dampened the drain by parasites. And this very efficient storage system doesn't have a relief valve. And it seems the efficient storage system leaks a little possibly causing constant damage.

A ferritin level of 55 was my goal, calculated by balancing the need for ferritin in an accidental blood loss with the danger posed by ferritin released with a heart attack/stroke. Maybe I should shoot for the low edge of the reference range.

Edited by david ellis, 02 October 2008 - 05:47 AM.

[david ellis]

When I started this topic, I was unsure about iron. Now I definitely side with the lower than average argument for longevity (for men) - based on research in the last year or so - and if I am getting iron, it would be nice to have only heme iron.

Mind, I was wondering why Christiaan Leeuwenburgh focused on heme and non-heme levels of iron. I didn't know how to use his findings about heme&non-heme iron. Especially after I found this article about non-heme ferritin produced abundantly by Helicobacter pylori. Adjusting your diet of plant based non-heme iron might not stop Helicobacter pylori from its abundant production(10 x normal). This is very interesting because all of this ties into the "inflammation" theory of heart disease. I saw one study that proved ROS iron damaged LDL. Helicobacter pylori is already implicated with heart disease. Oxidized LDL does damage the epithelial layer of the arteries. Its very interesting that ROS iron could be at the bottom of these problems.

Also the connection with sarcopenia caught my attention. At age 69 I have been looking for ways to battle that problem. All in all, Mind, thanks for the post you made.

So to find out if ferritin blood tests were of value I read his article on Medplus. From the article -
"Rikans et al. also concluded that the increased sensitivity of hepatocytes from old rats to diquat was not because of changes in enzymatic mechanisms that protect against oxidative damage; rather, they found that hepatocytes from old rats were more sensitive to diquat because of higher levels of ferritin iron in the livers of the old rats [59]. In addition, a clinical study in a large sample of Japanese men and women demonstrated that the oxidative DNA damage measured by circulating 8-oxoGuo levels increased concurrently with serum ferritin levels in both sexes "

The Japanese study, which Leeuwenburg referenced, confirms the use of ferritin to measure the ROS risk. So, ferritin, is an objective measure of ROS activity. Maybe not the best, but only $28 at LEF.

In the article he mentioned the difficulty of isolating the reactive iron from the un-reactive iron. That probably drove his decision to measure heme & non-heme iron.

Edited by david ellis, 02 October 2008 - 06:36 PM.

[stephen_b]

For anyone so inclined, you can calculate the number of donations it would take to take you from a starting level to an ending level by using the diffusion equation. I've attached a spreadsheet I made for that.

It doesn't take into account new iron from food, of course, and assumes that all iron is in the blood.

Stephen

Attached Files

•  Blood_donation_and_serum_iron_concentration.xls   28KB   218 downloads

[david ellis]

For anyone so inclined, you can calculate the number of donations it would take to take you from a starting level to an ending level by using the diffusion equation. I've attached a spreadsheet I made for that.

It doesn't take into account new iron from food, of course, and assumes that all iron is in the blood.

Stephen

Stephen, the graph was very close to my experience. A very handy chart.

[StrangeAeons]

Continuing in the "pro-iron" side of the debate, I should point out something the orthomolecular psychiatrist pointed out.
He ordered labs for TIBC, ferritin, and serum iron to to make sure he wasn't jumping the gun, but the doc claimed that many people (including men) suffer from iron deficiencies, and that hemoglobin and hematocrit would be the last things to show it. After understanding the ferritin storage system, I realize why this is so.

The doc gave me miscellaneous xeroxed pages of a biochem textbook showing metabolic pathways:

Evidently Fe3+ is essential for metabolism from Phenylalanine to Tyrosine to catecholamines (DOPA-> Dopamine -> Norepinephrine -> Epinephrine). Obviously dopamine and norepinephrine are very important neurotransmitters and a kink in their anabolism could show up as a cognitive deficit.

Likewise these charts also indicate that Fe2+ is essential for the conversion of Tryptophan to 5-HTP and Serotonin to 5-HIAA, so I imagine this means an iron deficiency would lead to fluctuations in serotonin, as Iron is essential for both the synthesis and breakdown of serotonin. I imagine this would lead to mood swings and possibly intermittent fatigue and anxiety.

Finally Fe2+ also appears to be responsible for the metabolism of choline, a substance which many of us here on the forums recognize as very valuable for cognition. Choline becomes betaine, which becomes DMG (dimethylglycine). DMG needs Fe2+ to become Sarcosine, and Sarcosine needs Fe2+ to become Glycine-- an amino acid that acts as a neurotransmitter.

I'm still wary of the guy, but as he put it, "textbook biochemistry doesn't lie". There's reason to believe iron plays a big role in the brain.

[niner]

I'm still wary of the guy, but as he put it, "textbook biochemistry doesn't lie". There's reason to believe iron plays a big role in the brain.

I haven't looked at the pathways, but one question to ask would be "does the iron act catalytically or is it consumed in the reaction?" If it's acting catalytically, then it's probably not going to be very sensitive to iron deficiency, because the enzymes that use the iron tend to hold on to it rather tenaciously. If it's consumed, then iron deficiency would probably be a big problem.

[StrangeAeons]

I haven't looked at the pathways, but one question to ask would be "does the iron act catalytically or is it consumed in the reaction?" If it's acting catalytically, then it's probably not going to be very sensitive to iron deficiency, because the enzymes that use the iron tend to hold on to it rather tenaciously. If it's consumed, then iron deficiency would probably be a big problem.

From what I can gather, tetrahydrobiopterin and Fe3+ are cofactors in catecholamine synthesis; but the fact that it's enzyme bound (by phenylalaine 4-hydroxylase and tyrosine hydroxylase) doesn't seem to differ from its role in hemoglobin formation (as it is bound to both heme and transferrin), and yet it's possible to get iron-deficient anemia.

Per my limited knowledge:
It would appear the main difference is that red blood cells last several months before they're lysed and the hemoglobin is seperated and metabolized, whereas catecholamines seem to be broken down and synthesized on a more regular basis (I'm thinking of the relatively short half-life of epinephrine administered medically or the relatively rapid efficacy of MAOI's); which, would then appear to make this proces more sensitive to iron deficiency.

On the other hand, while I have some vague medical training I am clearly out of my realm when it comes to biochemistry, so feel free to contradict me if you know otherwise.

As per the other Iron reactions I mentioned, I couldn't find specifics, though in my search on Choline metabolism I came across one of the same isolated pages out of the xeroxed textbooks, labelled "Property of the Metametrix Institute". This smells incredibly fishy, as it appears I'm being fed a standardized list of excerpts instead of the docs own personally selected and compiled materials. I don't know if I want to drink the Kool-Aid.

[VespeneGas]

This orthomolecular psychiatrist is quite interesting. I'm making some popcorn, pulling up a chair, and waiting for your judgment as to whether or not he's a quack.

[StrangeAeons]

This orthomolecular psychiatrist is quite interesting. I'm making some popcorn, pulling up a chair, and waiting for your judgment as to whether or not he's a quack.

It's a shame it takes forever to get an appointment with him; as far as I know, he's the only OM psychiatrist in the Indianapolis area, and quite possibly the state. He's quite a character; he looks a lot like Will Forte from SNL and is energetic on the verge of hyperactivity the way he moved around the desk bouncing from topics like methylation to minerals to amino acids to neurotransmitters, etc.
He has a master's in physiology, an M.D. and is double boarded in psychiatry and neurology; but while he seems to have a good knowledge of biochemistry, as a conventional doc he seems to be dropping the ball.
The sheet I got back from him claimed they did a survey for suicidal ideatiion-- a very obviously important aspect of a psychiatric assessment, and yet he made no such surveys. Likewise he used an ICD code for Autoimmune Disorder NOS even though he's actually hypothesizing an inflammatory issue; and the fact that he ordered C-Reactive Protein labs but not an Antinuclear Antibody Assay highlights this.
At this point I'm heavily debating whether or not I should just demand an MAOI from him (a dreadful oversight on behalf of the past 6 or 7 psychiatrists I've seen over the years, none of whom it ever occurred to to try one) or to try out his regimen, which he admitted off the cuff would take a long time to be effective. He also alluded to the notion that after following his regimen you can detect a release of BDNF (well, he said, "a protein that makes neurons grow") which makes me really skeptical. The fact that I'm beginning my highly stressful paramedic internship right now doesn't help the matter.

Going back to the iron issue, if the tests come back low than I suppose there might be something to his theory; on the other hand, them coming back normal proves very little. Notably, I've donated blood 4 times in the past year and haven't really noticed any change in mood subsequently aside from the obvious hypovolemic fatigue immediately afterwards; but the role of iron in NT synthesis would seem to inform the earlier post regarding iron and cognition.

[StrangeAeons]

Update: just donated blood again today and my hemoglobin was 12.9. I can't remember what it was last time, but I'm pretty sure it was in the 13's; I'm fairly sure it's been trending downwards. Evidently the normal range is 12.1-17, with 12.5 being the minimum to donate. I'm wondering if the downward trend is relevant to ferritin stores; I haven't gotten my iron, TIBC and ferritin labs back just yet, but I think investigating these values in neuropsychatiric disorders may be of value, even if normally iron is detrimental in men.
So to sum up: blind iron supplementation = detrimental
BUT: investigating iron deficiencies in neuropsychiatric disorders = worthwhile
supplementing iron in the event of a deficiency = no-brainer

[Skötkonung]

I have a hereditary disorder called hemochromatosis that causes my body to uptake and store iron at an abnormally fast rate. My mutation is homozygous C282Y. Untreated, the disease results in:

Malaise
Liver cirrhosis (with an increased risk of hepatocellular carcinoma)
Liver disease is always preceded by evidence of liver dysfunction including elevated serum enzymes specific to the liver.
Insulin resistance (often patients have already been diagnosed with diabetes mellitus type 2) due to pancreatic damage from iron deposition
Erectile dysfunction and hypogonadism, resulting in decreased libido
Congestive heart failure, arrhythmias or pericarditisArthritis of the hands (especially the first and second MCP joints), but also the knee and shoulder joints
Damage to the adrenal gland, leading to adrenal insufficiency
Deafness
Dyskinesias, including Parkinsonian symptoms
Dysfunction of certain endocrine organs:
Parathyroid gland (leading to hypocalcaemia)
Pituitary gland

Source:
http://en.wikipedia....Hemochromatosis

Sounds terrible, right? Fortunately it can be treated and normal or even extended life expectancy can be restored. If my serum transferrin and transferrin saturation are too high, I will undergo bi-weekly phlebotomy (blood donation) treatments until it is corrected. For maintenance purposes, I donate blood every 3-6 months, take inositol hexaphosphate with iron heavy meals (spinach, red meat, beans, etc), avoid vitamin C supplements (it increases iron absorption), and drink plenty of green and black tea as it has been shown to block iron absorption. These treatments have kept my transferrin and transferrin saturation on the low end of healthy and I have to becareful not to become aenemic.

A number of studies have been done on people with hemochromatosis and they have shown that reducing blood iron restores normal healthspan and life expectancy.

Survival and causes of death in hemochromatosis
http://www.ncbi.nlm..../pubmed/3389643

Associations of mutations in the hemochromatosis gene with shorter life expectancy
http://www.ncbi.nlm....pubmed/11700156

If you are worried about your iron levels, I would donate blood every two months and drink lots of tea.

[StrangeAeons]

My labs are in, and this is rather interesting, behold!

Iron, Total: 23 mcg/dL L
Ref: 30-160
Iron Binding Capacity, Unsaturated: 425 mcg/dL H
Ref: 110-370
TIBC: 448 mcg/dL H
Ref 228-428
Sat: 5% L
Ref: 7-70
Ferritin: 5.0 ng/mL L
Ref: 10.0-291.0

Conclusion: If you have refractory psych issues, this is clearly worth investigating.
EDIT: Evidently through some clerical error the lab thought I was a female. Obviously this indicates an even greater deficiency, though it did explain why my testosterone labs came back way out of reference range

Edited by PetaKiaRose, 06 February 2009 - 09:00 PM.

[ajnast4r]

wouldnt the logical solution to this problem be to just become a vegetarian?

I have a hereditary disorder called hemochromatosis that causes my body to uptake and store iron at an abnormally fast rate. My mutation is homozygous C282Y. Untreated, the disease results in:

Malaise
Liver cirrhosis (with an increased risk of hepatocellular carcinoma)
Liver disease is always preceded by evidence of liver dysfunction including elevated serum enzymes specific to the liver.
Insulin resistance (often patients have already been diagnosed with diabetes mellitus type 2) due to pancreatic damage from iron deposition
Erectile dysfunction and hypogonadism, resulting in decreased libido
Congestive heart failure, arrhythmias or pericarditisArthritis of the hands (especially the first and second MCP joints), but also the knee and shoulder joints
Damage to the adrenal gland, leading to adrenal insufficiency
Deafness
Dyskinesias, including Parkinsonian symptoms
Dysfunction of certain endocrine organs:
Parathyroid gland (leading to hypocalcaemia)
Pituitary gland

Source:
http://en.wikipedia....Hemochromatosis

Sounds terrible, right? Fortunately it can be treated and normal or even extended life expectancy can be restored. If my serum transferrin and transferrin saturation are too high, I will undergo bi-weekly phlebotomy (blood donation) treatments until it is corrected. For maintenance purposes, I donate blood every 3-6 months, take inositol hexaphosphate with iron heavy meals (spinach, red meat, beans, etc), avoid vitamin C supplements (it increases iron absorption), and drink plenty of green and black tea as it has been shown to block iron absorption. These treatments have kept my transferrin and transferrin saturation on the low end of healthy and I have to becareful not to become aenemic.

A number of studies have been done on people with hemochromatosis and they have shown that reducing blood iron restores normal healthspan and life expectancy.

Survival and causes of death in hemochromatosis
http://www.ncbi.nlm..../pubmed/3389643

Associations of mutations in the hemochromatosis gene with shorter life expectancy
http://www.ncbi.nlm....pubmed/11700156

If you are worried about your iron levels, I would donate blood every two months and drink lots of tea.

[Skötkonung]

wouldnt the logical solution to this problem be to just become a vegetarian?

Cutting down on meat intake may help slightly, but it is not an end-all solution. Even beans and dark leafy greens contain lots of iron. A low iron diet is not recommended or even possible to design. Iron is in everything and foods that contain iron also provide other essential elements to help heal and rebuild the body. Red meat is an important source of B vitamins. Fresh fruits and vegetables benefit the liver more than processed foods. I think a better approach to slow or stop the absorption. An example is taking IP6 with meals, donating blood regularly, etc.

Edited by shawn57187, 08 February 2009 - 01:06 AM.

[JLL]

Iron from plant sources (non-haem) is poorly absorbed, 5% or even less, whereas from meat (haem) 10-30% is absorbed. The absorption of non-haem iron can also be inhibited even further by things like green tea; with haem iron it's not so easy.

I don't advocate a vegetarian diet, but it is an effective way of lowering iron absorption.

[Skötkonung]

Iron from plant sources (non-haem) is poorly absorbed, 5% or even less, whereas from meat (haem) 10-30% is absorbed. The absorption of non-haem iron can also be inhibited even further by things like green tea; with haem iron it's not so easy.

I don't advocate a vegetarian diet, but it is an effective way of lowering iron absorption.

You're right, heme iron, which makes up 40 percent of the iron in animal tissue is well absorbed. Non-heme iron, which comprises the other 60 percent of the iron in animal tissue and all the iron in plants is less well absorbed. Vegan and vegetarian diets only contain non-heme iron. Because of this, you would think iron recommendations for vegetarians (including vegans) would be higher than for non-vegetarians. However, this is not the case. As my hematologist has indicated to me previously, the increased vitamin C content in a plant based diet elevates the bio-availability of non-heme iron. There for it would be a more accurate recommendation that one should avoid high sources of vitamin C with iron rich meals if you are looking to slow iron absorption.

...absorption. For example, iron supplementation may reduce zinc absorption, while excessive intakes of zinc can interfere with copper absorption. On the other hand, the absorption of iron from plants (nonheme iron) is enhanced when vitamin C is simultaneously present in the diet, and calcium absorption is improved by adequate amounts of vitamin D. Another key factor that influences mineral...

http://www.britannic...43/nonheme-iron

The reason for the satisfactory iron status of many vegans may be that commonly eaten foods are high in iron, as Table 1 shows. In fact, if the amount of iron in these foods is expressed as milligrams of iron per 100 calories, many foods eaten by vegans are superior to animal-derived foods. This concept is illustrated in Table 2. For example, you would have to eat more than 1700 calories of sirloin steak to get the same amount of iron as found in 100 calories of spinach.

Another reason for the satisfactory iron status of vegans is that vegan diets are high in vitamin C. Vitamin C acts to markedly increase absorption of non-heme iron. Adding a vitamin C source to a meal increases non-heme iron absorption up to six-fold which makes the absorption of non-heme iron as good or better than that of heme iron.

http://www.vrg.org/nutrition/iron.htm
http://www.ncbi.nlm..../pubmed/6764713

Edited by shawn57187, 09 February 2009 - 12:19 AM.