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Anemia isn't all about iron

All you ever hear "I am anemic, I HAVE to take iron." There is so much research out there that proves otherwise.



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."



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.


"Blood donors on average have superior health, but it's important to have good nutrition, because other nutrients are lost too."

—Ray Peat, PhD



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.


www.RayPeat.com

 

A fundamental problem with iron overload is the perturbed red(uction)ox(idation) balance that it creates and reinforces.


For example, cells get their energy from electrons derived from molecules such as sugar, fat, and protein. "Flowing" through the cell from protein to protein, electrons are eventually vacuumed into the loving arms of oxygen—the ultimate electron acceptor.


In a larger context, a body producing "efficient" respiratory energy (i.e., glucose to carbon dioxide) is in a highly oxidized "charged" state with few free electrons.[13]

Oxidation - The loss of electrons.Reduction - The gain of electrons.


When the ability to use oxygen has been interfered with, for example when the thyroid is suppressed and carbon dioxide is deficient, the flow of electrons "backs up" and leaks out of the mitochondria. These free highly reactive electrons tend to cause many unfavorable oxidative processes in the body (i.e. oxidative stress).


Moreover, a deficiency of oxygen requires the cell to find an alternative electron sink, as the increased reliance on glycolytic (or fermentation) metabolism forms far more electron carrying reduced NADH than oxidized NAD+.


The synthesis of fatty acids can serve as an alternative electron sink,[14] however, this poses many challenges for the metabolism, including the release of free iron,[15] which can greatly interfere with the functioning of the liver.[16,17]


The over-reliance on this "inefficient" janky fatty acid metabolism has been spun as a desirable trait by some health authorities, although, considering reductive excess is involved in just about every health problem (i.e., mitochondrial dysfunction), the idea seems highly dubious.


http://www.dannyroddy.com/weblog/ironoverloadredoxbalanceserotonin

 


Iron-copper interactions were described decades ago; however, molecular mechanisms linking the two essential minerals remain largely undefined. Investigations in humans and other mammals noted that copper levels increase in the intestinal mucosa, liver and blood during iron deficiency, tissues all important for iron homeostasis. The current study was undertaken to test the hypothesis that dietary copper influences iron homeostasis during iron deficiency and iron overload. We thus fed weanling, male Sprague-Dawley rats (n = 6-11/group) AIN-93G-based diets containing high (~8800 ppm), adequate (~80) or low (~11) iron in combination with high (~183), adequate (~8) or low (~0.9) copper for 5 weeks. Subsequently, the iron- and copper-related phenotype of the rats was assessed. Rats fed the low-iron diets grew slower than controls, with changes in dietary copper not further influencing growth. Unexpectedly, however, high-iron (HFe) feeding also impaired growth. Furthermore, consumption of the HFe diet caused cardiac hypertrophy, anemia, low serum and tissue copper levels and decreased circulating ceruloplasmin activity. Intriguingly, these physiologic perturbations were prevented by adding extra copper to the HFe diet. Furthermore, higher copper levels in the HFe diet increased serum nonheme iron concentration and transferrin saturation, exacerbated hepatic nonheme iron loading and attenuated splenic nonheme iron accumulation. Moreover, serum erythropoietin levels, and splenic erythroferrone and hepatic hepcidin mRNA levels were altered by the dietary treatments in unanticipated ways, providing insight into how iron and copper influence expression of these hormones. We conclude that high-iron feeding of weanling rats causes systemic copper deficiency, and further, that copper influences the iron-overload phenotype.



Fig 1 High-iron feeding impaired growth and caused cardiac hypertrophy.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4990348/

 

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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.

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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.

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

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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.

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

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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.

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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.

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