Iron's Dangers

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  1. charlie

    charlie The Law & Order Admin

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    Iron's Dangers
    http://raypeat.com/articles/articles/iron-dangers.shtml

    Q: You believe iron is a deadly substance. Why?

    Iron is a potentially toxic heavy metal. In excess, it can cause cancer, heart disease, and other illnesses.

    Q: Could you tell us about some of these studies?

    In the 1960s the World Health Organization found that when iron supplements were given to anemic people in Africa, there was a great increase in the death rate from infectious diseases, especially malaria. Around the same time, research began to show that the regulation of iron is a central function of the immune system, and that this seems to have evolved because iron is a basic requirement for the survival and growth of cells of all types, including bacteria, parasites, and cancer. The pioneer researcher in the role of iron in immunity believed that an excess of dietary iron contributed to the development of leukemia and lymphatic cancers. Just like lead, mercury, cadmium, nickel and other heavy metals, stored iron produces destructive free radicals. The harmful effects of iron-produced free radicals are practically indistinguishable from those caused by exposure to X-rays and gamma rays; both accelerate the accumulation of age-pigment and other signs of aging. Excess iron is a crucial element in the transformation of stress into tissue damage by free radicals.

    For about 50 years, it has been known that blood transfusions damage immunity, and excess iron has been suspected to be one of the causes for this. People who regularly donate blood, on the other hand, have often been found to be healthier than non-donors, and healthier than they were before they began donating.

    In one of Hans Selye's pioneering studies, he found that he could experimentally produce a form of scleroderma (hardening of the skin) in animals by administering large doses of iron, followed by a minor stress. He could prevent the development of the condition by giving the animals large doses of vitamin E, suggesting that the condition was produced by iron's oxidative actions.

    Excess iron's role in infectious diseases is now well established, and many recent studies show that it is involved in degenerative brain diseases, such as Parkinson's, ALS (Lou Gehrig's disease), Huntington's chorea, and Alzheimer's disease. Iron is now believed to have a role in skin aging, atherosclerosis, and cataracts of the lenses of the eyes, largely through its formation of the "age pigment."

    Q: How does excess iron accelerate our aging process?

    During aging, our tissues tend to store an excess of iron. There is a remarkably close association between the amount of iron stored in our tissues and the risk of death from cancer, heart disease, or from all causes. This relationship between iron and death rate exists even during childhood, but the curve is downward until the age of 12, and then it rises steadily until death. The shape of this curve, representing the iron burden, is amazingly similar to the curves representing the rate of death in general, and the rate of death from cancer. There is no other relationship in biology that I know of that has this peculiar shape, with its minimum at the age of 12, and its maximum in old age at the time of death.

    One of the major lines of aging research, going back to the early part of this century, was based on the accumulation of a brown material in the tissues known as "age-pigment." The technical name for this material, "lipofuscin," means "fatty brown stuff." In the 1960s, the "free radical theory" of aging was introduced by Denham Harman, and this theory has converged with the age-pigment theory, since we now know that the age-pigment is an oxidized mass of unsaturated fat and iron, formed by uncontrolled free radicals. Until a few years ago, these ideas were accepted by only a few researchers, but now practically every doctor in the country accepts that free radicals are important in the aging process. A nutrition researcher in San Diego suspected that the life-extending effects of calorie restriction might be the result of a decreased intake of toxins. He removed the toxic heavy metals from foods, and found that the animals which ate a normal amount of food lived as long as the semi-starved animals. Recently, the iron content of food has been identified as the major life-shortening factor, rather than the calories. [Choi and Yu, Age vol. 17, page 93, 1994.]

    Q: Exactly how much iron do we need to eat?

    Children's nutritional requirements are high, because they are growing, but there are indications that in the U.S. even children eat too much iron.

    Some researchers are concerned that the iron added to cereals is contributing to the incidence of leukemia and cancers of the lymphatic tissues in children. [Goodfield, 1984.] During the time of rapid growth, children are less likely than adults to store too much iron. At birth, they have a large amount of stored iron, and this decreases as they "grow into it." It is after puberty, when growth slows and the sex hormones are high, that the storage of iron increases. [Blood, Sept., 1976.] In a study of the "malnourished" children of migrant fruit pickers in California, these children who were "seriously anemic" were actually more resistant to infectious diseases than were the "well nourished" middle class children in the same region.

    If the normal amount of dietary iron causes an increased susceptibility to infections even in children, and if a subnormal amount of iron slows the aging process, I think we are going to have to reconsider our ideas of nutritional adequacy, to look at the long range effects of diet, as well as the immediate effects. My current studies have to do with analyzing our ability to handle stress safely, in relation to our diet. I believe our nutritional recommendations for iron have to be revised sharply downward.

    Q. Don't women need extra iron?

    That's a misunderstanding.

    Doctors generally don't realize that only a few milligrams of iron are lost each day in menstruation. The real issue is that you can hardly avoid getting iron, even when you try.

    Women absorb iron much more efficiently than men do. From a similar meal, women will normally absorb three times as much iron as men do. When pregnant, their higher estrogen levels cause them to absorb about nine times as much as men. Every time a woman menstruates, she loses a little iron, so that by the age of 50 she is likely to have less iron stored in her tissues than a man does at the same age, but by the age of 65 women generally have as much excess iron in their tissues as men do. (During those 15 years, women seem to store iron at a faster rate than men do, probably because they have more estrogen.) At this age their risk of dying from a heart attack is the same as that of men. Some women who menstruate can donate blood regularly without showing any tendency to become anemic.

    Since the custom of giving large iron supplements to pregnant women has been established, there has been an increase in jaundice of the newborn. It has been observed that women who didn't take iron supplements during pregnancy have healthy babies that don't develop jaundice. I have suggested that this could be because they haven't been poisoned by iron. Those supplements could also be a factor in the increased incidence of childhood cancer.

    Q: Don't you need iron supplements if you are anemic?

    In general, no.

    Many doctors think of anemia as necessarily indicating an iron deficiency, but that isn't correct. 100 years ago, it was customary to prescribe arsenic for anemia, and it worked to stimulate the formation of more red blood cells. The fact that arsenic, or iron, or other toxic material stimulates the formation of red blood cells doesn't indicate a "deficiency" of the toxin, but simply indicates that the body responds to a variety of harmful factors by speeding its production of blood cells. Even radiation can have this kind of stimulating effect, because growth is a natural reaction to injury. Between 1920 and 1950, it was common to think of "nutritional growth factors" as being the same as vitamins, but since then it has become common to use known toxins to stimulate the growth of farm animals, and as a result, it has been more difficult to define the essential nutrients. The optimal nutritional intake is now more often considered in terms of resistance to disease, longevity or rate of aging, and even mental ability.

    An excess of iron, by destroying vitamin E and oxidizing the unsaturated fats in red blood cells, can contribute to hemolytic anemia, in which red cells are so fragile that they break down too fast. In aging, red cells break down faster, and are usually produced more slowly, increasing the tendency to become anemic, but additional iron tends to be more dangerous for older people.

    Anemia in women is caused most often by a thyroid deficiency (as discussed in the chapter on thyroid), or by various nutritional deficiencies. Estrogen (even in animals that don't menstruate) causes dilution of the blood, so that it is normal for females to have lower hemoglobin than males. Q. What should I do if my doctor tells me I'm anemic? Is there any situation in which a person needs to take iron supplements?

    Iron deficiency anemia does exist, in laboratory situations and in some cases of chronic bleeding, but I believe it should be the last-suspected cause of anemia, instead of the first. It should be considered as a possible cause of anemia only when very specific blood tests show an abnormally low degree of iron saturation of certain proteins. Usually, physicians consider the amount of hemoglobin or of red cells in the blood as the primary indicator of a need for iron, but that just isn't biologically reasonable.

    If a large amount of blood is lost in surgery, a temporary anemia might be produced, but even then it would be best to know whether the iron stores are really depleted before deciding whether an iron supplement would be reasonable. Liver (or even a water extract of wheat germ) can supply as much iron as would be given as a pill, and is safer.

    Q. What foods contain iron?

    Flour, pasta, etc., almost always contain iron which has been artificially added as ferrous sulfate, because of a federal law. Meats, grains, eggs, and vegetables naturally contain large amounts of iron. A few years ago, someone demonstrated that they could pick up a certain breakfast cereal with a magnet, because of the added iron. Black olives contain iron, which is used as a coloring material. You should look for "ferrous" or "ferric" or "iron" on the label, and avoid foods with any added iron. Many labels list "reduced iron," meaning that iron is added in the ferrous form, which is very reactive and easily absorbed.

    Q.: Why does federal law require the addition of iron to those foods?

    Industrially processed grains have most of the nutrients, such as vitamin E, the B vitamins, manganese, magnesium, etc., removed to improve the products' shelf life and efficiency of processing, and the government required that certain nutrients be added to them as a measure to protect the public's health, but the supplementation did not reflect the best science even when it was first made law, since food industry lobbyists managed to impose compromises that led to the use of the cheapest chemicals, rather than those that offered the greatest health benefits. For example, studies of processed animal food had demonstrated that the addition of iron (as the highly reactive form, ferrous sulfate, which happens to be cheap and easy to handle) created disease in animals, by destroying vitamins in the food. You should read the label of ingredients and avoid products that contain added iron, when possible.

    Q: Can cooking in an iron frying pan put iron into food?

    Yes, especially if the food is acidic, as many sauces are. The added iron will destroy vitamins in the food, besides being potentially toxic in itself.

    Q: What about aluminum?

    Aluminum and iron react similarly in cells and are suspected causes of Alzheimer's disease.

    The aluminum industry started propagandizing more than 50 years ago about the "safety" of aluminum utensils, claiming that practically none of the toxic metal gets into the food. Recent research showed that coffee percolated in an aluminum pot contained a large amount of dissolved aluminum, because of coffee's acidity.

    Q: What kind of cooking pots or utensils are safe?

    Glass utensils are safe, and certain kinds of stainless steel are safe, because their iron is relatively insoluble. Teflon-coated pans are safe unless they are chipped.

    Q: How do I know which stainless steels are safe?

    There are two main types of stainless steel, magnetic and nonmagnetic. The nonmagnetic form has a very high nickel content, and nickel is allergenic and carcinogenic. It is much more toxic than iron or aluminum. You can use a little "refrigerator magnet" to test your pans. The magnet will stick firmly to the safer type of pan.

    Q: Why is there iron in most multi-vitamin and mineral products?

    Although several researchers have demonstrated that iron destroys vitamins, there is enough wishful thinking in industry, government, and the consuming public, that such mistakes can go on for generations before anyone can mobilize the resources to bring the truth to the public. 10 years ago, I thought it was a hopeful sign of increased awareness of iron's danger when the manufacturer of a new iron product mentioned in the Physician's Desk Reference that it hadn't yet been reported to cause cancer.

    Q. I can't avoid all those foods, especially the bread and grains. What can I do to keep the iron I ingest from harming me?

    Iron destroys vitamin E, so vitamin E should be taken as a supplement. It shouldn't be taken at the same time as the iron-contaminated food, because iron reacts with it in the stomach. About 100 mg. per day is adequate, though our requirement increases with age, as our tissue iron stores increase. Coffee, when taken with food, strongly inhibits the absorption of iron, so I always try to drink coffee with meat. Decreasing your consumption of unsaturated fats makes the iron less harmful. Vitamin C stimulates the absorption of iron, so it might be a good idea to avoid drinking orange juice at the same meal with iron-rich foods. A deficiency of copper causes our tissues to retain an excess of iron, so foods such as shrimp and oysters which contain abundant copper should be used regularly.

    Q: How does copper help us?

    Copper is the crucial element for producing the color in hair and skin, for maintaining the elasticity of skin and blood vessels, for protecting against certain types of free radical, and especially for allowing us to use oxygen properly for the production of biological energy. It is also necessary for the normal functioning of certain nerve cells (substantia nigra) whose degeneration is involved in Parkinson's disease. The shape and texture of hair, as well as its color, can change in a copper deficiency. Too much iron can block our absorption of copper, and too little copper makes us store too much iron. With aging, our tissues lose copper as they store excess iron. Because of those changes, we need more vitamin E as we age.

    SUMMARY:

    Iron is a potentially toxic heavy metal; an excess can cause cancer, heart disease, and other illnesses.

    Other heavy metals, including lead and aluminum, are toxic; pans and dishes should be chosen carefully.

    Iron causes cell aging.

    Drinking coffee with iron rich foods can reduce iron's toxic effects.

    Use shrimp and oysters, etc., to prevent the copper deficiency which leads to excess storage of iron.

    Avoid food supplements which contain iron.

    Take about 100 units of vitamin E daily; your vitamin E requirement increases with your iron consumption.


    GLOSSARY:

    Free radicals are fragments of molecules that are very destructive to all cells and system of the body.

    Respiration refers to the absorption of oxygen by cells, which releases energy. The structure inside the cell in which energy is produced by respiration is called the mitochondrion. Oxidation refers to the combination of a substance with oxygen. This can be beneficial, as in normal respiration that produces energy, or harmful, as in rancidity, irradiation, or stress reactions. Antioxidants: Vitamin E and vitamin C are known as antioxidants, because they stop the harmful free-radical chain reactions which often involve oxygen, but they do not inhibit normal oxidation processes in cells. "Chain breaker" would be a more suitable term. It is often the deficiency of oxygen which unleashes the dangerous free-radical processes. Many substances can function as antioxidants/chain breakers: thyroxine, uric acid, biliverdin, selenium, iodine, vitamin A, sodium, magnesium, and lithium, and a variety of enzymes. Saturated fats work with antioxidants to block the spread of free-radical chain reactions. Age pigment is the brown material that forms spots on aging skin, and that accumulates in the lens of the eye forming cataracts, and in blood vessels causing hardening of the arteries, and in the heart and brain and other organs, causing their functions to deteriorate with age. It is made up of oxidized unsaturated oils with iron.

    Anemic means lacking blood, in the sense of not having enough red blood cells or hemoglobin. It is possible to have too much iron in the blood while being anemic. Anemia in itself doesn't imply that there is nutritional need for iron.

    REFERENCES

    Allen, D. R., et al., "Catechol adrenergic agents enhance hydroxyl radical generation in xanthine oxidase systems containing ferritin: Implications for ischemia reperfusion," Arch. Biochem. Biophys. 315(2), 235-243, 1994.

    M. Bartal, et al., "Lipid peroxidation in iron deficiency anemia--Reply," Acta Haematol. 91(3), 170, 1994.

    R. J. Bergeron, et al., "Influence of iron on in vivo proliferation and lethality of L1210 cells," J. Nutrition 115(3), 369-374, 1985.

    P. Carthew and A. G. Smith, "Pathological mechanisms of hepatic tumor formation in rats exposed chronically to dietary hexachlorobenzene," J. Applied Toxicology 14(6), 447-52, 1994.

    Chen, Y., et al., "Weak antioxidant defenses make the heart a target for damage in copper-deficient rats," Free Radical Biol. Med. 17(6), 529-536, 1994.

    J. J. C. Chiao, et al., "Iron delocalization occurs during ischemia and persists on reoxygenation of skeletal muscle," J. Lab. Clin. Med. 124(3), 432-438, 1994.

    Choi, J. H. and B. P. Yu, "Modulation of age-related alterations of iron, ferritin, and lipid peroxidation in rat serum," Age 17(3), 93-97, 1994.

    P. C. Elwood, "Iron, magnesium, and ischemic heart disease," Proc. of Nutrition Society 53(3), 599-603, 1994.

    J. Goodfield, An Imagined World, Penguin Books, N.Y., 1984.

    M. Galleano and S. Puntarulo, "Mild iron overload effect on rat liver nuclei," Toxicol. 93(2-3), 125-34, 1994.

    E. C. Hirsch, "Biochemistry of Parkinson's disease with special reference to the dopaminergic systems," Mol. Neurobiol. 9(1-3), 135-142, 1994.

    G. M. Kainova, et al., "Activation of endogenous lipid peroxidation in the brain during oxidation stress induced by iron and its prevention by vitamin E," Bull. Exp. Biol. & Med. 109(1), 43-45, 1989.

    S. Kiechl, et al., "Body iron stores and presence of carotid atherosclerosis--results from the Bruneck study," Arterioscler. Thromb. 14(10), 1625-1630, 1994.

    A. V. Kozlov, et al., "Role of endogenous free iron in activation of lipid peroxidation during ischemia," Bull. Exp. Biol. Med. 99(1), 1984.

    D. J. Lamb and D. S. Leake, "Iron released from transferrin at acidic pH can catalyse the oxidation of low density lipoprotein," FEBS Lett 352(1), 15-18, 1994.

    E. E. Letendre, "Importance of iron in the pathogenesis of infection and neoplasm," Trends in Biochemical Sci., April, 1985, 166-168.

    V. M. Mann, et al., "Complex 1, iron and ferritin in Parkinson's disease substantia nigra," Ann. of Neurology 36(6), 876-81, 1994.

    Z. Maskos and W. H. Koppenol, "Oxyradicals and multivitamin tablets," Free Radical Biol. & Med. 11, 669-670, 1991.

    S. Ozsoylu, "Lipid peroxidation in iron deficiency anemia," Acta Haematol. 91(3), 170, 1994.

    Pecci, L., et al., "Aminoethylcystein ketimine decarboxylated dimer protects submitochondrial particles from lipid peroxidation at a concentration not inhibitory of electron transport," Biochem. Biophys. Res. Commun. 205(1), 264-268, 1994.

    M. Savoiardo, et al., "Magnetic resonance imaging in progressive supranuclear palsy and other parkinsonian disorders," J. Neural Trans. (suppl. 42), 93-110, 1994.

    J. J. Strain, "Putative role of dietary trace elements in coronary heart disease and cancer," Brit. J. Biomed. Sci. 51(3), 241-251, 1994.

    Vanrensburg, S. J., et al., "Lipid peroxidation and platelet membrane fluidity--implications for Alzheimer's disease?", Neuroreport 5(17), 2221-2224, 1994.

    L. J. Wesselius, et al., "Increased release of ferritin and iron by iron-loaded alveolar macrophages in cigarette smokers," Amer. J. Respir. Crit. Care Med. 150(3), 690-695, 1994.

    Transfusions: Amer. J. of Surgery 155, p. 43, 1988. *A Finnish study, two years ago, indicated that high iron stores may increase heart attack risk: In People magazine, 1994: "Is iron a killer?" Dr. Jerome L. Sullivan, director of clinical labs of Veterans Affairs Medical Center at Charleston, S.C., in 1983 proposed that excess iron contributes to heart attacks. University of Kuopio in Finland: Large-scale study (nearly 2,000 men, for up to five years; next to smoking, excess stored iron is the most significant identifiable risk factor for heart attacks. It is a stronger risk factor for heart attack than high blood pressure and cholesterol.

    *Dec. 7, page 6E, Register Guard (Eugene, OR): US studies showed a weak connection between iron and heart disease, and a weak connection with the iron in red meat. Epidemiologists at the Pacific Northwest Laboratory in Washington have reported that the greater the concentration of iron in a person's blood, the greater his or her risk of cancer. Richard Stevens and his co-workers found the connection from examining cancer rates in more than 8,000 people who participated in the l971 National Health and Nutrition Examination survey. A second Finnish study with similar findings accompanied Stevens's report in the International Journal of Cancer, and suggets that there may be cause for concern. Register Guard (Eugene, OR), Jan. 16, 95; p 7A: Number of heart failures doubles, AP: 1982-92, heart disease death rate dropped 24.5%; number of cases of congestive heart failure doubled during roughly the same period. It killed 39,000 Americans in 1991, costs system $40 billion per year. Cancer is the biggest killer of women under 64, heart disease far surpasses cancer in women of ages 65-84.
     
  2. Amazoniac

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    Youtube: iron cereal magnet
     
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    Aarghhh! Looks like the road to hell is paved with iron!
     
  5. Amazoniac

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    When there's excess muscle breakdown from stress hormones, are the organs overflooded with iron even if you don't ingest any?
     
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  11. Amazoniac

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    I was producing a consideration if it's reasonable to restrict iron at all costs for a few days after a blood donation [yo] to force drawing from the reserves instead of relying on a help from diet for red bloody cells formation.

    Lorfutanely, it appears that the amounts that foods are able to provide are nowhere near the amount lost, but given that extra iron shorten the 'recovery' period and that it can take months for restoration, diet also counts. The doses used below are massive, but the process speeds up depending on the amount supplied.

    It's not something to be concerned because with repeated losses the risk of a depletion for someone who eats a diet with normal amounts are real.

    - Rate of blood regeneration after blood loss

    Summary:
    "The rate of blood regeneration following blood loss has been quantitatively determined in man. Blood production is proportional to the amount of available iron, whether derived from iron stores or from iron ingestion. There may be a depletion of body iron stores despite normal peripheral blood values. In such instances, bleeding results in little or no increase in blood production. On the other hand, adequate available iron permits an acceleration of hemopoiesis to two to three times the normal rate. The variability from two or three weeks to three or four months in recovery from a 500 ml. phlebotomy may be explained on the basis of variable iron stores. When supplementary iron is given, phlebotomies may be performed every two weeks without the production of significant anemia. Since the peripheral blood values give no indication of iron stores, it seems advisable to provide supplemental iron therapy to all blood donors. If this is done, the interval between blood donations need be no more than two to three weeks."


    "Estimates of recovery time range from a few days 1 to several months.[2] Marked individual variation is found within any one group of donors; for example, Fowler and Barer[2b] noted recovery times of from 21 to 98 days among 63 subjects."

    "Large amounts of plasma protein and hemoglobin must be synthesized to replace the deficit produced by phlebotomy. Plasma protein is rapidly regenerated and repeated phlebotomies have not produced significant depletion in normal subjects; 1,000 ml. of plasma removed over a period of six hours was largely replaced in one week (Chart 1). Other reports 10 also indicate that weekly phlebotomies do not produce significant plasma protein deficits. This would be anticipated from studies of turnover rate of plasma proteins,[11] indicating a normal turnover rate of plasma proteins 5 to 10 times that of hemoglobin. Reserve stores of mobilizable protein have also been demonstrated in animals 12 and man.[13] It is concluded that replacement of plasma protein following phlebotomy is of no concern. It is to be emphasized that this conclusion pertains only to normal subjects on normal diets. Two instances of protein depletion have been observed by us following phlebotomies in chronic alcoholics with cirrhosis, and instances have been reported in malnournished subjects.[14]"

    Hematocrit - Wikipedia

    "The hematocrit (/hɪˈmætəkrɪt/) (Ht or HCT), also known by several other names, is the volume percentage (vol%) of red blood cells in blood. It is normally 47% ±5% for men and 42% ±5% for women."
    "The essential factors in erythropoiesis [red blood cell formation] are the stimulus for blood production, the functional capacity of the marrow, and the available supplies of building materials."

    "The intensity of stimulus for erythropoiesis may be assumed to be inversely proportional to the hematocrit level. [A signal from a drop after blood donation for example] This has been illustrated by studies of bleeding in dogs[15] and by the bone-marrow-inhibiting effect of transfusions.[16] It is also evident in these studies that, while an average time of 40 days is required to regenerate 500 ml. of blood,[2b] 3,500 ml. of blood was replaced in normal subjects in 100 to 120 days."

    "The demand placed on the marrow for regeneration of a 500 ml. phlebotomy in one week is a hemopoietic rate of one and one-half times normal. Since in hemolytic anemias various measurements of hemopoiesis indicate rates of blood production of 5 to 10 times normal,[17] the demands imposed in this study on the bone marrow would be expected to lie well within marrow capacity. The difference between these conditions is that hemolytic anemias do not result in a loss of the products of red cell catabolism from the body. It would not be unexpected therefore that deficiency in a building material might be the limiting factor in hemopoiesis following blood loss. This deficiency is in iron."

    "In evaluating response to phlebotomy the first consideration is the iron-depleted subject. It has previously been shown that 80 to 90 days are required in depleted patients with polycythemia vera to replace the erythrocytes removed in 500 ml. of blood.[9] If blood loss from menstruation or other causes is superimposed on exhausted iron stores, even longer time would be required."

    "While the normal subject has a much greater capacity to regenerate blood, this capacity is proportional to his iron reserve. Persons with normal hematological findings may have depleted stores, normal stores, of 1 to 1.5 gm., or stores of much greater size.[18] An approximation of the size of these stores can be made by sternal marrow examination.[19]"

    upload_2019-1-17_13-22-57.png
    "If iron deficiency is obviated by administration of iron, the studies reported provide a format of the rates of hemopoiesis and the severity of anemia with different quantities of blood-letting. In male subjects bled 500 to 1,000 ml. weekly a packed red cell mass of about 35% (deficit of 10%) and a hemopoietic rate of twice normal were found. Subjects bled 500 ml. weekly demonstrated a packed red cell mass of 37.5% (deficit of 7.5%) and hemopoiesis one and one-half to two times normal. In subjects bled 500 ml. every two weeks a packed red cell mass of 42% (deficit of 3%) and a hemopoietic rate of one and one-half times normal were found. The values for packed red cell mass would be 3% lower in women. Definite symptoms of anemia were found with depression of the hematocrit level of 10%, mild symptoms between 5 and 10%, and no symptoms when the deficit was less than 5%."

    "It is apparent that supplemental iron therapy must be given to insure rapid regeneration of blood after phlebotomy. The data of Barer and Fowler and of Santy[20] indicate that complete replacement will then occur within one month. Our data indicate that if iron is taken continuously 500 ml. phlebotomies may be performed as often as every two weeks for many months without the development of sufficient anemia to produce symptoms. Even at weekly intervals phlebotomies will be tolerated with only moderate anemia and borderline symptoms."

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    upload_2019-1-17_13-24-58.png
    "In most of the reports of regeneration after phlebotomy it is emphasized that females may be slow in replacement of blood.[21] In view of the smaller iron stores and the frequent mild iron deficiency anemia in the female[20a] this would be expected. Menstruation is important not so much in terms of the increased blood production required but in terms of the iron depletion which it effects. It is in the female blood donor that routine iron therapy would appear to be most useful."​

    - Adverse reactions and iron deficiency after blood donation

    "Dietary iron is absorbed by enterocytes in the duodenum and proximal jejunum. Absorption is tightly regulated because iron in excessive amounts is toxic to cells (e.g., by generation of ferric peroxides and free radicals) and there is no defined mechanism of excretion. Iron from animal sources (heme iron) is more bioavailable (∼35% absorbed) than nonheme iron (vegetable sources:∼10% absorbed).[47] Men normally absorb ∼1 mg/day, equaling basal losses from the GI tract and skin. Iron absorption in premenopausal women is∼0.5 mg/ day greater, because of additional losses from menstruation. Absorption capacity increases in proportion to the level of iron deficiency (Figure 5.3), reaching a maximum that averages 4–5 mg/day in frequent donors,[48,70] and is enhanced with supplemental iron.[49]"

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    "Iron not directly utilized in physiologic pathways is stored in tissues as ferritin; small amounts present in blood are in equilibrium with tissue ferritin, which is considered a reliable indicator of available storage iron, especially in healthy blood donors, who have low rates of inflammatory conditions that can result in elevated ferritin values irrespective of iron status.[52] The total body iron content in men averages approximately 50 mg/kg (~4000 mg), whereas women have 35 mg/kg (~2500 mg). The majority of the total (70–80%) exists in red blood cells bound to hemoglobin. Approximately 10% of body iron is engaged in other cellular physiologic functions, such as enzymes and cytochromes, or bound to transferrin. Only 10–20% of the total is present in the form of tissue iron stores that are available for erythropoiesis and metabolic use. Cook et al. estimated tissue iron stores of 776±313mg in men and 309±346mg [?] in women.[53] The loss of approximately 230mg iron with each whole blood donation along with the limited stores and capacity for absorption lead to a high incidence of iron deficiency in frequent donors, especially women."


    "The “classic” cutoff [ferritin] value, 12 ng/ml, has been utilized as a specific but insensitive indicator of absent iron stores in the clinical setting[59] and in blood donors.[60] One study found that this cutoff failed to identify iron depletion in over one-third of cases in blood donors.[61] Two clinical studies based largely on bone marrow staining for iron have found 15 ng/ml to more accurately reflect iron deficiency anemia.[62,63]"

    "Iron depletion begins with the gradual loss of storage iron, a relatively small compartment as indicated above. Once stores are exhausted, a phase of IDE[rythropoesoaipdgsis] ensues, which then progresses to iron-deficiency anemia (IDA).[68] Iron deficiency is prevalent in the US population as a whole, especially among premenopausal women, in whom survey data reveal ferritin values <15 ng/ml in 14% of women aged 12–49.[58] In first-time blood donors, iron deficiency (defined as ferritin 12 ng/ml) is rare in men (under 1%) and reported in 6.6–12% overall.[46,66] Nearly 70% of the 9 million blood donors who donate annually in the United States are repeat donors, who are especially subject to iron depletion.[1] The prevalence of iron deficiency (using ferritin 12 ng/ml) reported in repeat donors ranges from 6 to 16% in men and from 28 to 63% in women.[60,66] Overall, using the most sensitive laboratory measures, iron depletion (defined as iron levels associated with impaired erythropoiesis; see below [No, (Wagner, 2018).]) is estimated to affect as much as 25–35% of the entire donor population.[88,89] Even individuals who exclusively donate by plateletpheresis may develop low iron because of the increased frequency allowed and fixed red blood cell losses occurring with each procedure (50–80 ml in samples and tubing).[90]"

    "Low hemoglobin, a late consequence of iron deficiency, is the most common reason for donor deferral, with nearly 7% of presenting donors not allowed to donate because they cannot meet the minimum capillary hemoglobin standard of 12.5 gm/dl.[1] Hemoglobin deferral disproportionately affects women, with 17.7% of presenting women and 1.6% of men deferred.[91] Using the WHO defined thresholds of 13 gm/dl in men and 12 gm/dl in women, by definition, all men who are deferred are anemic, as are those women with hemoglobin values below 12 mg/dl. Prevalence estimates of iron depletion are high in hemoglobin-deferred donors. In one study, 53% of women and 61% of the men had iron measurements below lower gender-based limits.[92] The prevalence of iron depletion in controls (nondeferred donors) was also quite high in the study, reflecting the poor correlation of hemoglobin with iron status. Consistent with these findings, an Australian study of premenopausal women found mean ferritin to be lower in hemoglobin-deferred donors, 8.4 ng/ml, versus 27 ng/ml in women who were not deferred (p <0.0001).[93]"

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    "Pica is an eating disorder characterized by the compulsive ingestion of nonfood substances—mostly ice (pagophagia), but including other substances such as chalk, clay, or uncooked starch—that also has been strongly associated with iron deficiency.[109] In the RISE study, pica symptoms were found in 6% of donors when surveyed at end of study, and in a multivariate analysis was eight times more common in women who had ferritin 12 ng/ml than in iron-replete women.[103] At the NIH, pica was found in 11% of iron-depleted or -deficient donors (ferritin <20 ng/ml in women and <30 ng/ml in men) compared to 4% of iron-replete donors(p<0.0001). Pica symptoms resolved generally within two weeks of starting oral iron therapy.[102] Pica symptoms predominated in female donors in these studies."

    "Observational studies suggest that prolonging the interdonation interval reduces the risk of iron depletion in blood donors. The RISE study found that interdonation intervals of less than 14 weeks were associated with increased risk of low hemoglobin deferral (OR∼2–2.5) and iron deficiency (OR∼3–4.4 for ferritin <12 μg/L), and concluded that lengthening the minimum interval would reduce the risk of iron depletion.[89] However, because 39% of donors in RISE acknowledged taking some form of iron supplements, iron ingestion (and not simply waiting longer between donations) may also have played a role in shortening the period of iron recovery."

    "A study in very frequent blood donors of both sexes (men up to six times and women up to four times per year) who were randomized to 40 mg, 20 mg, or placebo ferrous gluconate found that the ferritin levels remained low but were maintained in donors who received 20 mg daily but declined in the placebo controls.[135] Positive iron balance (increased ferritin) was observed only in donors taking 40 mg daily."

    "In the HEIRS trial, compared to donors who did not take iron, donors taking iron supplements had a significantly shorter time to hemoglobin recovery in both the low-ferritin (mean 32 days vs. 158 days) and higher ferritin groups (31 days vs. 78 days).[126] The accelerated hemoglobin recovery from iron supplements was seen in donors with ferritin values up to 50 ng/ml, or higher than expected based on pre-donation ferritin. This is because of the iron deficit induced by blood donation, essentially lowering ferritin in some donors to iron-deficient levels post donation (ferritin <26 ng/ml; Figure 5.6), thus delaying their erythropoietic recovery. Above a ferritin of 50 ng/mL, donors no longer recovered hemoglobin any faster on iron supplements. With iron tablets, iron stores recovered in about 11 weeks, slightly longer than the current eight-week waiting period for donors to be eligible to donate again. Without iron, two-thirds of the donors did not recover the iron they lost by the end of the study in 24 weeks."

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  12. Amazoniac

    Amazoniac Member

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    There's more or less 5 liters of blood in a pimp/pimpess.
    With the information above, 75% of the body iron is found in it.
    For someone having 4000 mg of total iron, that's 3000 mg in the bloody.
    500 ml of blood expulsion represents 10% of the blood volume, so 10% of 3000 mg: 300 mg.
    Now you have 1000 mg + 2700 mg.

    If you begin to adsorb 4 mg from your diet after the procedure −1 (Travo, 2018) mg from usual loss, that's 350 mg in 4 months. This coincides with the normalizations above but not with the drop in ferritin. What's likely to be occurring instead is that the body senses the drop, signals release from reservoir because it can't absorb enough from a normal diet for restoration, and from the amount released it starts to make a kick the production and slowly decreases the adsorption. In other words, a great deal must come from storage.
     
  13. Orius

    Orius Member

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    Too much focus on one factor: iron.

    The body needs ceruloplasmin to oxidize ferrous iron (iron II) to ferric iron (iron III), which is also less accessible to infectious organisms because iron III can be more readily sequestered by the ferritin protein. Ceruloplasmin is part of the ferroxidase complex in the body that accomplishes this.

    Ceruloplasmin relies on bioavailable copper and whole food vitamin C (not ascorbic acid) to be formed. Whole food C has tyrosinase at its core, which is comprised of bioavailable copper. Magnesium is also a key factor in displacing unbound iron from tissues.

    Without adequate ceruloplasmin, whole food C and magnesium, iron remains in ferrous form, remains unbound, and causes oxidative damage to the tissues. Most people in modern society are lacking in bioavailable copper and magnesium. Taking a copper supplement won't work, it'll just increase toxic copper in the body, no different than if you regularly drink water from copper pipes. Organic copper is found in things like sesame seeds, shellfish, bovine liver, etc.

    If you flood a person's body with unbound iron and they are lacking in these important co-factors, then they will develop iron related diseases. It's why some people can get iron IVs and be just fine while others feel sick for days. The African studies are a reflection of this. People are poor and malnourished, so of course iron is going to feed infections. The people have no co-factors to buffer the unbound iron so that pathogenic organisms can't access it. Cancers work the same way. When the body develops cancer, it starts pumping out ferritin to sequester the iron from the cancer; but the ferritin can't bind the iron without ceruloplasmin.
     
  14. Amazoniac

    Amazoniac Member

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    That sounds very good in theory, but in practice we find that people in health circles are already eating fine diets and still have problems with iron accumulation from inflammation, often involving infections that can be present anywhere throughout the digestive tract or inside the body.

    While we keep theorizing about it, it keeps building up and worsening the inflammation. It's reasonable to control the excess with blood loss until you fix the cause, unless you's already anaemic. If ferritin is elevated due to inflammation, you'll worsen it before you normalize ferritin.

    There have been people with elevated blood ferritin that decreased their levels to 50 ng/ml with some donations and they were expected to reaccumulate their stores requiring further donations in the future, but on tests they found out that iron stayed on the desirable range. So it was not mere management, it was part of the correction for them.


    - Iron deficiency or anemia of inflammation?: Differential diagnosis and mechanisms of anemia of inflammation

    "Iron deficiency (ID) can occur in two major forms: absolute and functional ID. Both forms of ID can manifest either isolated or combined, and will result in iron-deficient erythropoiesis and, if unrecognized or left untreated, in anemia [1, 2].

    Absolute ID, as defined by a decrease in the body’s iron content, usually develops when the absorption of dietary iron in the duodenum and proximal jejunum (Fig. 1a) cannot compensate for an increased iron demand or blood loss. Despite adaptive induction of expression of the transmembrane iron transporters divalent metal transporter (DMT)-1 and ferroportin (FPN)-1 in enterocytes upon ID, iron absorption can only be increased by 2‑ to 3‑fold to approximately 5 mg per day [3, 4]. Due to this relatively inefficient process, iron stores, particularly ferritin-associated iron in liver and spleen, can become depleted during chronic bleeding episodes, repetitive blood donations, helminth infestations, through materno-fetal transfer, or during growth [5]."

    "Under homeostatic conditions, the absorption of 1–2 mg of iron per day compensates for its loss via desquamation of epithelial cells from skin and mucosal membranes and during menstrual bleeding. The majority of the 20–25 mg of iron required for daily erythropoiesis is provided by the degradation of effete RBC and the iron contained within their Hb (Hemoglobin)."

    "Following immune activation by pathogen- or damage-associated molecular patterns, the interaction of myeloid cells with T and B lymphocytes results in the generation of pro- and anti-inflammatory cytokines. These divert iron fluxes from the circulation to storage sites by controlling the expression of HAMP, of iron transporters, and of the iron-storage protein FT. Therefore, duodenal iron absorption and macrophage iron recycling are reduced, the serum becomes iron-starved and the erythron lacks sufficient iron for proliferation and hemoglobin synthesis. Therefore, zinc may replace iron as the central heme-cation. Zinc protoporphyrin-IX (not depicted) can be measured to confirm the presence of this mechanism of iron sequestration."

    "Inadequate iron absorption has also been found in association with Helicobacter pylori infection, hypergastrinemia, celiac disease, or vitamin D deficiency [9, 10]. Prolonged ID results in the inability to regenerate skin and mucosal membranes and in iron deficiency anemia (IDA) with its classical symptoms such as fatigue."

    "Functional ID has a more complex pathophysiology and is commonly defined as a redistribution of iron from the key sites of its utilization (erythron, epidermis, mucosal surfaces) to storage sites, particularly the hepatic and splenic mononuclear phagocyte system (MPS). Moreover, in states of increased erythropoiesis such as during therapy with erythropoiesis-stimulating agent (ESA) or after major blood loss, erythropoiesis may become iron-restricted so long as the mobilization of storage iron cannot catch up with its demand for hemoglobin (Hb) synthesis (see the interpretation of CHr (Content of reticulocyte hemoglobin), HYPO (Hypochromic erythrocytes), and ZnPP (Zinc protoporphyrin) in diagnostic section). The ultimate consequence of these functional disturbances of iron homeostasis is anemia, which is often referred to as anemia of inflammation (AI) or anemia of chronic disease (ACD)."

    "Absolute and functional iron deficiency may also coexist. Such combined conditions render the interpretation of erythrocyte indices and parameters of iron status challenging."

    "ID results in difficulties regenerating epidermis and mucosal epithelia, while also affecting the clinical course of associated chronic diseases. For instance, ID has negative effects on mitochondrial respiration and tissue oxygen consumption and, thus, on cardiac function and the clinical course of congestive heart failure (CHF) [16–18]. The importance of anemia for CHF is underscored by a linear increase of mortality with declining Hb levels [19–21]."

    "AI can be viewed as a spectrum of acute and chronic forms of anemia whose common pathophysiological denominator is their occurrence as a result of immune activation [25, 26]."

    "Acute and chronic infections, inflammatory disorders, and malignancies are the principal disease types underlying AI."

    "In addition, combined forms of IDA and AI may be present. This scenario is typically observed in inflammatory bowel disease (IBD) or gastrointestinal or urogenital malignancy. Mucosal erosions and ulcerations are associated with recurrent bleeding episodes and lead to a substantial loss of iron, since 0.5 mg of iron are contained within the Hb of 1 ml of blood. At the same time, the underlying disease provides an inflammatory stimulus for the sequestration of iron in the MPS. Moreover, menstruation, hemodialysis, the requirement for repetitive blood sampling, and anticoagulant or antiplatelet drugs may contribute to iron loss in CKD and other chronic diseases."

    "The excessive production of inflammatory mediators diverts iron to the MPS, rendering it relatively unavailable for erythroid progenitors [33]. A paradigm for such a mediator is hepcidin anti-microbial peptide (HAMP). HAMP is the hormonal negative-feedback regulator of serum iron, as it limits iron-fluxes to the circulation. Upon iron excess or inflammation, HAMP is produced by hepatocytes and, in much smaller quantities, by immune cells and other cell types."

    "For instance, lipopolysaccharide as a component of the Gram-negative cell wall enhances HAMP production while stimulating DMT1 expression in myeloid cells, thereby favoring iron sequestration [35]."

    "The liver is a key organ initiating and maintaining AI [12]. Hepatocytes are the key source of HAMP, while Kupffer cells (KC) are a major site of inflammation-driven iron storage. Interestingly, KC dampen HAMP production in homeostatic conditions but may be required for inflammation-driven HAMP secretion [44, 45]."

    "In their reproductive years, women have an increased iron demand. Estradiol, whose levels increase after menstrual bleeding during the first half of the menstrual cycle (follicular phase) until ovulation, inhibits HAMP transcription in hepatocytes, which may allow for higher intestinal iron absorption to compensate for the average 20–80 ml of monthly menstrual blood loss [73, 74]. In contrast, progesterone, which rises after ovulation and dominates the second half of the cycle (luteal phase) until menstrual bleeding, rather stimulates HAMP expression [75]. Given the resulting fluctuations of HAMP and iron indices, the last five days of the menstrual cycle have been proposed for blood sampling to allow for a more representative evaluation of iron status in women [76]."

    "The spleen contributes to the pathogenesis of AI as site of iron retention in macrophages. Furthermore, splenomegaly may result in hypersplenism and a reduced half-life of red blood cells (RBC) as a consequence of the increased RBC elimination by red pulp macrophages (RPM)."

    "Numerous infectious agents (e. g., parvovirus B19 and human herpes virus-6) and neoplastic cells may infiltrate the bone marrow, which eventually disturbs erythropoiesis by several mechanisms, including direct damage to erythroid cells and putative negative effects on the microenvironment and the stem cell niche."

    "While in its classical form AI constitutes a hyporegenerative anemia, hemolysis may contribute to the development of AI or aggravate its degree in several settings. For instance, several bacteria including Staphylococcus aureus produce hemolysins [98]. These destroy RBC, liberating heme for its uptake into bacteria by specific receptors. Different mechanisms of heme iron acquisition are exploited by intraerythrocytic infectious agents such as Plasmodium [99]."

    "In addition, the life span of circulating RBC may be negatively affected by inflammatory mediators such as TNF and by mechanical stress [104]."

    "Similar to the concurrent presence of absolute ID in the setting of AI, deficiencies in other nutrients essential to erythropoiesis, such as folate and vitamin B12, may be contributory. For instance, celiac disease may cause profound malassimilation of various nutrients or poor food intake may aggravate the anemia of the elderly."

    "Since the AI is a direct consequence of an active immune-driven disease, its first-line therapy is treatment of the underlying condition."

    "It is generally assumed, similar to the hypoferremia of the acute phase response, that AI is the pathophysiological consequence of the body’s attempt to reduce the availability of iron for infectious agents."​
     
  15. Orius

    Orius Member

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    50ng/L or lower is reasonable. Some groups say 20 or lower is ideal but I find this rather quacky. My internist said that 100ng is optimal and everyone should be there. For me this would be iron overload. However, some people naturally get to that point, which calls into question why their bodies allow higher levels of they don't have problems with hepcidin as in hemochromotosis. There must be an individual basis for this.

    I'm lucky in that I have access to all my blood work since I was 14 years old. My natural range is 30-45. My colleague said he starts to feel deficient below 60.

    This past year due to a bleeding disorder my ferritin dropped to 3. I didn't start feeling normal until it got to at least 30.

    Bottom line, I believe in the intelligence of the body. Unless one has hemochromotosis, or is receiving iron parenterally, the body will set its own natural levels. I don't understand why blood letting is necessary in most cases, unless there's something like polycythemia happening.
     
  16. dbh25

    dbh25 Member

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    I started with ferritin above 200. Then donated blood every 8-10 weeks until it fell in the 20s. I donated 4x the next year, then 6 months later, I felt wiped out with a ferritin of 15. I had not taken any iron supplements.
    I wish I knew the above info at the time, and donated 1-2x per year. The hematocrit number they check was always in the acceptable range to give blood.
     
  17. Amazoniac

    Amazoniac Member

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    'maasai drinking blood' :handok:
     
  18. sugarbabe

    sugarbabe Member

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    Maasai also drink milk. The calcium would help in not absorbing too much iron.
     
  19. Amazoniac

    Amazoniac Member

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    Michelle, there's a snake not wanting me to post.

    I tried but couldn't find information on milch inhibition of heme iron adsorption. It makes no sense to try to prevent it if they could simply consume less or not at all, unless they're after other stuff in blood but I'm not sure about this. Perhaps it has to do with protecting too much iron throughout the digestive chanelle.

    It's easy to find videos of tribal gurus consuming straight blood like savages.
    They scare the cattles with a jugular puncture but do them a favor because they don't kill them, it's just an occasional blood donation.

    Some of them drink the blood after clothing it after cooking or agitation while (I assume) discarding the coagulate with straining. Maybe it's more fluid this way and easier to combine with milk to form the strawberry-milk concussion.

    - Zebu cattle weight: 250 kg
    - 14 liters of blood
    - 14 g total iron (50-60 ppm of weight)
    - 10 g/14 liters*
    - 350 mg/500 ml.

    *It was taking too much time to find out, I used human proportions which might be off, but must not be too far off given the amount of blood and total iron.

    It's difficult to know how much they drink, but I would guess it's around 100 ml from the videos available, so they might get 35 mg of heme iron each time.

    Also related, if blood volumes for men and women are more or less similar, what likely varies the most is the stored iron. So using the same proportion will give you a worse estimate. They claimed the range of iron found in blood in relation to total is 70-80%, so for a pimp I would use 70%, and 80% for a pimpess since she has less stored.
     
  20. Amazoniac

    Amazoniac Member

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    Advanced Nutrition and Human Metabolism' (978-1-133-10405-6):

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