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SOME IRON FACTIODS:
The average adult male has about 4.5 grams of iron in the body.
Iron is distributed in six areas of the body:
- Hemoglobin – about 3000 mg (66.4 %)
- Myoglobin – about 160 mg (3.5 %)
- Storage Iron (Ferritin, Hemosiderin) – about 1125 mg in men (25 %), 650 mg in women
- Tissue Iron – about 110 mg (2.5%) This includes ron-containing enzymes such as the cycochromes, peroxidases, catalse, oxidases, dehydrogenases
- Transport iron (transferrin) – about 4.5 mg (0.1 %)
- Labile Iron pool – about 110 mg (2.5 %). This is ion that is temporarily bound to cell membrane or cytoplasmic proteins before being incorporated into heme, enzymes or other structures
The body can only absorb about 1 mg out of every 20 mg of iron in food consumed.
- Ferric iron is not absorbable
- Ferrous iron is absorbable
Total daily iron loss is
- about 1 mg/day in 70-kg men and
- 0.8 mg/day in 55-kg non-menstruating females,
- 1.2 to 3.4 mg/day in menstruating females
USA Food and NUtrition Board Recommended daily allowance of iron:
- Adult males 8 mg/day,
- adolescent males 11 mg/day,
- adult females premenopausal 18 mg/day, adult females postmenopausal 8 mg/day,
- adolescent females 15 mg/day,
- pregnant females 27 mg/day
Vegetarian diet contains less absorbable iron.
The adjusted US RDA adjusted for vegetarian diet is:- men 14 mg/day,
- postmenopausal women 14 mg/day,
- premenopausal women 33 mg/day,
- adolescent females 26 mg/day
Regular intense exercise increases iron requirements by about 30%.
1 Unit of Blood contains 250 mg iron.
1 unit blood donation in susceptible women, 3-4 units of blood donation in men may exhaust iron stores.CAUSES OF IRON DEFICIENCY:
Iron deficiency may occur from the sum of iron intake and iron losses as follows:INADEQUATE IRON IN FOOD
- Minerally deficient farmland leads to mineral deficient fruits and vegetables
- Lack of meat, seafood – both promote absorption of non-heme iron. Meat provides well-absorbed heme iron.
- Vegetarian diet – iron from plant sources are less efficiently absorbed
POOR ABSORPTION OF IRON
- Diarrhea
- Malabsorption Syndrome (e.g. gastric bypass)
- Hiatal Hernia
- Celiac Disease
- Inadequate Gastric Acid (improves iron absorption by converting ferric iron to ferrous form)
- Aging
- Antacid use (reduces absorption of iron, zinc, etc.)
- Coffee/Caffeine (causes loss of B-vitamins, Vitamin C, calcium, iron and zinc)
- Inadequate Vitamin C (improves iron absorption by converting ferric iron to ferrous form)
- Inadequate sugar (glucose, fructore), amino acids, succinates (these bind to iron and facillitate binding to intestinal mucosa, which absorbs the iron).
- Excess pancreatic alkaline secretions (convert ferrous iron to inasorbable ferric form)
- Dietary phosphates in cereals bind to iron and prevent absorption
- Phytates (inositol hexaphosphate salts) are in grains, seeds, nuts, vegetables, roots (e.g. potatoes), and fruits
- High phytate content: bran, whole-wheat flour, oats.
- Coffee, Tea, Cocoa contain Polyphenols (such as tannin), which bind to iron, preventing absorption
- Calcium competes with iron for absorption. Maximal inhibition of iron is 60% by 300-600 mg of calcium in a meal.
- Fermented vegetables – enhance iron absorption
- Red wine (most) contain phenolic compounds which bind iron and inhibit absorption
- Certain medications impair iron absorption (e.g. Tetracycline)
BLOOD LOSS
- Gastrointestinal bleed (more than 50 causes)
- Aspirin, Ibuprofen and other NSAIDS)
- Ulcerative Colitis
- Gastric Ulcer
- Hook Worm
- Colon Cancer
- Hemorrhoids
- Hereditary Hemorrhagic telangiectasia (Osler’s disease)
- Renal loss (hematuria,
- Menstruation
- Fibroids
- Endometriosis
- Post-partum hemorrhage
- Dialysis
- Hemolysis
- Malaria
- G6PD deficiency
IUD Use
- Intense Exercse (e.g. marathon running).
- Exercise decreases intestinal blood flow by 20-50%,
- Decreased blood flow increases the risk of ischemic damage to the stomach and intestin.
- Exercise also decreases lower esophageal sphincter pressure, increasing the risk of erosive esophagitis.
- Running may traumatize gastrointestinal organs and increase the risk of bleeding from hemorroids.
PHYSIOLOGIC LOSS OF IRON
- Menstruation
- Sweat
- Urine
- Bile
- Loss of skin cells
- Loss of cells from mucosal membrane, stomach, and intestines.
INCREASED IRON REQUIREMENTS
- Growth (expansion of the total body iron body)
- Pregnancy and lactation
It has been seen in many people that have low thyroid that low ferritin levels exist. Some times correcting the thyroid correct the anemia, but in others iron supplementation must be administered to correct the imbalance. Would the reason for this be a down regulation in the enyzme iron transferase that uptakes iron into the tssue. Is not proper amounts of copper needed to help the body to convert iron from ferric to ferrous in order for it to be loaded on the protein enyzme ceruloplasm?
@hardasnails1973 343 wrote:
It has been seen in many people that have low thyroid that low ferritin levels exist. Some times correcting the thyroid correct the anemia, but in others iron supplementation must be administered to correct the imbalance.
Would the reason for this be a down regulation in the enyzme iron transferase that uptakes iron into the tssue.
Is not proper amounts of copper needed to help the body to convert iron from ferric to ferrous in order for it to be loaded on the protein enyzme ceruloplasm?
Low thyroid and low iron can often be comorbid conditions.
Low thyroid hormone may impair iron absorption by decreasing the metabolism of gastrointestinal mucosal cells.
Low iron would also impair metabolic processes signaled by thyroid hormone, including thyroid hormone production, itself.
Thus, one has a vicious circle by having one or the other condition promoting problems with the other.
—
I am not sure if “iron transferase” is down-regulated or is involved. If it is, then I would expect an iron overload problem, rather than an iron deficiency.
As far as I know:
In the intestinal mucosal membrane enterocytes, DMT1 (Divalent Metal Transporter 1) transports Ferrous Iron (Fe2+) from the intestinal lumen, across the cell membrane, into the enterocyte cytoplasm. DMT1 is regulated by iron levels in the body. It is increased when iron is deficient. The ferrous iron then diffuses through the cytoplasm into the blood side. There it is transported through the cell membrane by ferroportin, is oxidized to ferric iron (Fe3+), by hephaestin, a membrane-bound ferroxidase. Ferric iron (Fe+) is then bound to plasma Transferrin for distribution to the rest of the body. Hephaestin is similar to Ceruloplasmin, though is membrane bound. Another enzyme, Xanthine Oxidoreductase, which is 1000 times more potent than Ceruloplasmin, which does not contain copper, may also be involved in the oxidation of iron in the enterocyte.
Copper is needed to produce Ceruloplasmin. Ceruloplasmin, not only transports copper in the blood (as part of its structure it contains 6 copper atoms), but it also oxidizes iron, converting it from the ferrous iron (Fe 2+) to the ferric iron (Fe3+) form. The ferric iron form is the only form of iron that Transferrin can bind to. Transferrin then delivers iron to the rest of the body through the blood. Without Ceruloplasmin, iron can’t be transported. And iron storage in the liver, brain and pancreas becomes overloaded, causing damage.
@DrMariano 344 wrote:
Low thyroid and low iron can often be comorbid conditions.
Low thyroid hormone may impair iron absorption by decreasing the metabolism of gastrointestinal mucosal cells.
Low iron would also impair metabolic processes signaled by thyroid hormone, including thyroid hormone production, itself.
Thus, one has a vicious circle by having one or the other condition promoting problems with the other.
—
I am not sure if “iron transferase” is down-regulated or is involved. If it is, then I would expect an iron overload problem, rather than an iron deficiency.
As far as I know:
In the intestinal mucosal membrane enterocytes, DMT1 (Divalent Metal Transporter 1) transports Ferrous Iron (Fe2+) from the intestinal lumen, across the cell membrane, into the enterocyte cytoplasm. DMT1 is regulated by iron levels in the body. It is increased when iron is deficient. The ferrous iron then diffuses through the cytoplasm into the blood side. There it is transported through the cell membrane by ferroportin, is oxidized to ferric iron (Fe3+), by hephaestin, a membrane-bound ferroxidase. Ferric iron (Fe+) is then bound to plasma Transferrin for distribution to the rest of the body. Hephaestin is similar to Ceruloplasmin, though is membrane bound. Another enzyme, Xanthine Oxidoreductase, which is 1000 times more potent than Ceruloplasmin, which does not contain copper, may also be involved in the oxidation of iron in the enterocyte.
Copper is needed to produce Ceruloplasmin. Ceruloplasmin, not only transports copper in the blood (as part of its structure it contains 6 copper atoms), but it also oxidizes iron, converting it from the ferrous iron (Fe 2+) to the ferric iron (Fe3+) form. The ferric iron form is the only form of iron that Transferrin can bind to. Transferrin then delivers iron to the rest of the body through the blood. Without Ceruloplasmin, iron can’t be transported. And iron storage in the liver, brain and pancreas becomes overloaded, causing damage.
So if one had low ceruloplasmin plasma this could potentially lead into a situation that would be similar to hemochromatosis. Would there be any other markers in the blood to distinguish this from copper deficiency vs wilsons diseae? One would think that if iron gets build up in the tissue that ferritin levels would go up and not down. If I am understanding this right if ceruloplasmin is low this would hinder iron to be transported into ferritin which is stored form resulting in excessive oxidation stress to the body. The tricky thing about this is that low copper and wilson’s disease both have low ceruloplasmin which makes it hard to distinguish. Also high consumption of zinc can also give a similar scenerio. Would looking at zinc and copper ratio in the serum give a better indication of this? What is the least amount of zinc that could off set a copper deficeincy? I have read as little as 15 mgs a day with out copper can cause a zinc:copper imbalance. The thing is I always have low ceruloplasmin and copper serums even before I start supplementing zinc which was clinically deficient which concerns the fact of potentially wilson’s disease. The most startling thing was that i was taken copper 5 mgs up untill the day before the test even and still tested low levels.
Please bare with me as I am still trying to learn the biochemistry of how ceruloplasmin can affect iron metabolism. This part of the puzzle has always caught my attention to potentially holding the link to many unanswered question. My hair analysis showed low copper and iron despite proper ferritin levels 5 years ago. The hair analysis shows that despite proper ferritin levels in the blood and low ceruloplasm I have low tissue levels of iron and copper. Since the hair is usually last place for minerals to get stored this may have some validation of why I feel anemic, despite adequete b-12, folate, ferritin levels. Its the iron (ferritin) is not getting transported to the tissue due to the low ceruloplasmin. While being hypothyroid is causing ferritin levels to be unstable because of the slow uptake from the intestinal tract. This could also explain reducing zinc to 30 mgs a day for 3 months ,using 5 mgs of copper, reducing vitamin C the ceruloplasm or copper serums never changed. My conclusion is that from ruling out 3 months of proper zinc:copper, lower vitamin C with no change in serum copper or ceruloplasmin that there is something else responsible.
Could low cholesterol levels be some how linked genetically with this since bile is needed to eliminate excessive copper? I have had low cholesterol all my life and I have a theory that my levels are low due to the fact that my body is making bile at the expense of other hormones. I am on now TRT because of this low cholesterol which even when I was 16 years old was 99. The dr’s told me I was the best they have seen.
My first serum readings 5 years ago after supplementing 5 mgs of copper and <30 mgs of zinc for 3 months were 16 ceruloplasmin (18-36) and just recently 20 (19-36) and copper serum 73 (70-150) supplementing 30 mgs of zinc a day no copper
This is the stuff that scares me
http://www.ebmonline.org/cgi/content/full/232/2/323
When looking at symptoms of wilsons diseae I fall into vast majority of them both psychological and physical plus I have a few markers for it as well.Dr. Mercola thinks the optimal ferritin level is between 40-80
@BlackJack 394 wrote:
Dr. Mercola thinks the optimal ferritin level is between 40-80
Dr. Mercola isn’t a psychiatrist.
As a psychiatrist, I optimize for behavior.
Optimizing for behavior is a higher, more stringent standard than the standard used to treat physical health. For example, I evaluate and treat for diabetes in childhood, not in adulthood, as with general physicians. I would assess for and treat pre-diabetes, not leaving as an active problem. Pre-diabetes, to me is just as bad as diabetes in contributing to the development of mental illness. I would treat thyroid problems at an earlier stage than a general physician would should it be part of the pathophysiology of the patient’s mental illness. Since the underlying causes of mental illness are the same for many physical illnesses, I want to see a person be physically well in order to achieve mental wellness.
Given a recent study where senior citizens can have impaired red blood cell production at a ferritin below 75, I don’t think levels below 75 are optimal.
I generally see behavioral improvements when iron is optimized to a ferritin level of 150 for men, and 100-120 for women.
In the scheme of things, an optimum male ferritin level of 150 is still at the midrange, with levels above the upper end of 300 clearly indicating hemochromatosis.
Once a ferritin level is found over 300, then further assessment needs to be done. Iron overload can occur with excessive dietary iron. It can occur with hereditary hemochromatosis.
In regard to iron overload is: http://www.hemochromatosis.org/
My iron is 100. I want to go to 150 in ferritin. How much time to go at this level ? How much can I take ? What the best brand ?
Thank@Jean 598 wrote:
My iron is 100. I want to go to 150 in ferritin. How much time to go at this level ? How much can I take ? What the best brand ?
ThankProbably the best way is to have a nutrient dense diet with animal sources of protein. Beef with the fat is a good source of iron.
Iron is also available in over-the-counter supplements. Ferrous Sulfate is probably the most commonly used supplement.
It usually takes months to improve Ferritin.
It is very important to do this with a medical provider’s supervision, with regular ferritin measurements since excessive iron is very destructive. It is also important to coordinate iron with the rest of one’s treatment to minimize interactions. For example, iron can bind to thyroid hormone and reduce its absorption.
I was taking Cypress Ferrous Fumarate 324 mg, Two Tablets /day it works great I am told one needs to get 200 mgs. of mg Elemental Iron per day. I was on this about 6 months my levels come up good and I felt much better. But it was very hard on my stomach after taking it this long I started to get some bad heartburn. Because the type of Iron supplement is genital on the stomach we never figured it was the iron pills.
In trying to find out way the Heartburn we found I had 2 blockages to my heart and got Heart bypass sugary. After all the surgery’s I was told to go back on the Iron pills. I was on them not a week and the heartburn come back.
So now I take this and it cost more money but works much better and does not upset my stomach.
Feosol Carbonyl Iron Supplement 2 tables a day.
PhilWhen a person presents with high ferritin levels , but normal hemocrit, RBC, low % iron saturation levels could this be a biological response to a hidden infection some where in the body? Could dehydration also cause alteration in iron metabolism? The person is complaining of thicken semen with yellow tint, but not painful ejaculation. I recommended that he go to urologist, and GI specialist to rule out intestinal bleeding, also get second opinon for hemochromatosis. CBC do not represent any abnormal indication of acute or low grade infection. The hemotologist is scratching hes head and does not believe it was hemochromatosis. When a person is on TRT for a while and CBC gets altered how long will it take to return to normal base line?
@pmgamer18 657 wrote:
I was taking Cypress Ferrous Fumarate 324 mg, Two Tablets /day it works great I am told one needs to get 200 mgs. of mg Elemental Iron per day. I was on this about 6 months my levels come up good and I felt much better. But it was very hard on my stomach after taking it this long I started to get some bad heartburn. Because the type of Iron supplement is genital on the stomach we never figured it was the iron pills.
In trying to find out way the Heartburn we found I had 2 blockages to my heart and got Heart bypass sugary. After all the surgery’s I was told to go back on the Iron pills. I was on them not a week and the heartburn come back.
So now I take this and it cost more money but works much better and does not upset my stomach.
Feosol Carbonyl Iron Supplement 2 tables a day.
Philgood information to have. I was on supplement and it made me sick with diarhea. I will try this.
It comes in 2 box’s so I do a searh when I need more and always find this to be the best price I am now on 3 pills / day this is working great for me.
http://www.amazon.com/Feosol-Ferrous-Sulfate-Supplement-Therapy/dp/B001G7QLYA/ref=pd_sbs_hpc_2Thanks Phil, you’re a gem!!
I’m going to be having ALOT of things shipped to my hotel in Seattle! Shipping to Canada is so expensive.
I can’t wait to get all my orders and have my “New Beginning”Here’s an interesting article I read on Celtic Sea Salt
http://www.visualizationworks.com/featureseasalt.htm
I posted it on the other site as well. I am so thankful for these sites- I really feel like I am on the way to a new me!
@pmgamer18 1179 wrote:
It comes in 2 box’s so I do a searh when I need more and always find this to be the best price I am now on 3 pills / day this is working great for me.
http://www.amazon.com/Feosol-Ferrous-Sulfate-Supplement-Therapy/dp/B001G7QLYA/ref=pd_sbs_hpc_2Articles of biological impact due to unhealthy levels of ferritin and iron storage
@hardasnails1973 1321 wrote:
Articles of biological impact due to unhealthy levels of ferritin and iron storage
The abstracts to the articles above are as follows:
Thyroid. 2002 Oct;12(10):867-78.Related Articles, Links
The impact of iron and selenium deficiencies on iodine and thyroid metabolism: biochemistry and relevance to public health.
Zimmermann MB, Köhrle J.
Laboratory for Human Nutrition, Swiss Federal Institute of Technology, Zürich, Switzerland. Michael.zimmermann@ilw.agrt.ethz.ch
Several minerals and trace elements are essential for normal thyroid hormone metabolism, e.g., iodine, iron, selenium, and zinc. Coexisting deficiencies of these elements can impair thyroid function. Iron deficiency impairs thyroid hormone synthesis by reducing activity of heme-dependent thyroid peroxidase. Iron-deficiency anemia blunts and iron supplementation improves the efficacy of iodine supplementation. Combined selenium and iodine deficiency leads to myxedematous cretinism. The normal thyroid gland retains high selenium concentrations even under conditions of inadequate selenium supply and expresses many of the known selenocysteine-containing proteins. Among these selenoproteins are the glutathione peroxidase, deiodinase, and thioredoxine reductase families of enzymes. Adequate selenium nutrition supports efficient thyroid hormone synthesis and metabolism and protects the thyroid gland from damage by excessive iodide exposure. In regions of combined severe iodine and selenium deficiency, normalization of iodine supply is mandatory before initiation of selenium supplementation in order to prevent hypothyroidism. Selenium deficiency and disturbed thyroid hormone economy may develop under conditions of special dietary regimens such as long-term total parenteral nutrition, phenylketonuria diet, cystic fibrosis, or may be the result of imbalanced nutrition in children, elderly people, or sick patients.
Iron deficiency anemia and catecholamine metabolism
PATIROGLU T. ; DOGAN P. ;
Erciyes univ. medical fac., dep. pediatrics biochemistry, Kayseri 38039, TURQUIEAbstract:
To assess the effects of iron therapy on platelet monoamine oxidase (MAO) activity and urinary excretion of total metanephrines (MN) in infants and young children with iron deficiency anemia, 24 subjects were tested before and after one month of oral iron treatment. Thirteen healthy children comprised the control group. In the control group, platelet MAO level was 0.21±0.02 U/mg protein (mean ± SE), urinary total metanephrine was 2.51±0.47 μg/mg creatinine. In cases with iron deficiency, mean platelet MAO level was 47.6 % lower (p0.05) than the control valuesIndian pediatrics ISSN 0019-6061 CODEN INPDAR
1991, vol. 28, no1, pp. 51-56 (17 ref.)
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