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jimmylegs wrote:i'm already sure that excess iron is as much a problem as deficiency.

i'm curious to discover whether taking iron to correct a deficiency state can simultaneously equate to overload heart disease and oxidation (rust).

Prevalance of Iron deficiency anemia: In the United States, 20% of all women of childbearing age have iron-deficiency anemia, compared with only 2% of adult men. (Source: excerpt from Anemia: NWHIC)

Deaths from Iron deficiency anemia: 118 deaths (NHLBI 1999)

soils... mineral or organic, are inundated with water, anaerobic conditions usually result... rate at which oxygen can diffuse through the soil is drastically reduced.
Low diffusion rate leads relatively quickly to anaerobic, or "reduced", conditions, with the time required for oxygen depletion on the order of several hours to a few days after inundation begins.
rate at which oxygen is depleted depends on the ambient temperature... sometimes the chemical oxygen demands from reductants such as ferrous iron.

oxidation: electrons are lost (oxygen uptake, hydrogen removal)
reduction: electrons are gained (oxygen release, hydrogen uptake)

there is a predictable thermodynamic sequence of reduction. it starts with nitrogen, then manganese, then iron.
iron going from ferric to ferrous form:
Fe(OH)3 + e^- + 3H^+ ---> Fe^2+ + 3H2O

...redox potentials are not precise thresholds, because pH and temperature are also important factors...

Not only is iron common, but it is also reactive and readily reflects changes in surrounding Eh/pH conditions. This is particularly true in soil and groundwater systems that have been environmentally impacted with hydrocarbons. In groundwater systems iron occurs in one of two oxidation states: reduced soluble divalent ferrous iron (Fe+2) or oxidized insoluble trivalent ferric iron (Fe+3). The modern atmosphere has 21% oxygen, causing most of the iron in shallow subsurface soils to be in the oxidized ferric state.

Many important biological processes involve redox reactions.
Cellular respiration, for instance, is the oxidation of glucose (C6H12O6) to CO2 and the reduction of oxygen to water. The summary equation for cell respiration is:
C6H12O6 + 6 O2 ? 6 CO2 + 6 H2O

The goal of iron chelation therapy is to prevent iron-mediated injury to cells. The basis of this injury is the very property that makes iron vital to all life: it can exist in either of two stable oxidation states. Iron ions in aqueous solution exist either in the ferrous (Fe2+) state or the ferric (Fe3+) state. The shift of electrons between iron and donor molecules is the basis of energy production by controlled oxidation of carbohydrates, proteins, and lipids. Iron is a key element in most of the cytochrome enzymes involved in the oxidative phosphorylation of the Krebs cycle.
Because of its ability to participate in chemical reactions that involve the shift of electrons between molecules (reduction-oxidation or redox reactions), the body tightly regulates iron. When iron is tightly bound to a chelator molecule, be it a protein or a small chemical, the reactivity of the iron is greatly dampened. The key iron storage protein in the body is ferritin. Ferritin is a very large spherical molecule (6). Iron is deposited as semi-crystalline deposits inside these protein "vaults". Iron that is sequestered within ferritin is metabolically inactive.
The iron deposits in patients who have received multiple blood transfusions for chronic anemia, such as thalassemia, can exceed the storage and detoxification capacity of ferritin. Consequently, "free" (or more accurately, loosely bound) iron begins to accumulate in tissues and blood. This "free" iron can catalyze the formation of very injurious compounds, such as the hydroxyl radical (.OH) from compounds such as hydrogen peroxide, which are normal metabolic byproducts (Fenton reaction) (7).

Iron absorption occurs primarily in the duodenum. Most of this
iron is in the ferric (+++) form and is complexed to other organic
and inorganic molecules. The acid in the stomach and hydrolytic
enzymes in the small intestine release the iron from these
complexes. It is then reduced to the ferrous (++) form as it is
more readily absorbed in this state. Absorption is increased by
the presence of:
glucose
fructose
some amino acids
ascorbic acid (Vitamin C)
These substances aid in the absorption process by either reducing
ferric iron to the ferrous state or by helping bind the iron to the
mucosal cell receptor sites. It is recognition of the positive
effects of vitamin C which has resulted in many iron supplements
being manufactured with this vitamin present. Heme iron, iron in
meat myoglobin, is more easily absorbed than elemental iron. Iron
absorption is decreased by the presence of:
phosphate
bicarbonate
bile acids
Once the ferrous iron (++) binds to receptors on the surface of
mucosal cells it is moved into the cell. This is an energy dependent
process. In the mucosal cell the iron is oxidized back to the
ferric (+++) state and bound to apoferritin in the cell. This
continues until all the apoferritin bound at which point newly
absorbed iron is no longer oxidized but rather is passed through
the cell and into the portal circulation still in the ferrous
state. In the blood, iron is bound to transferrin in the ferric
state. Bound to transferrin, the iron is transported to the marrow
for use or storage.

Co-supplementation of ferrous salts with vitamin C exacerbates oxidative stress in the gastrointestinal tract leading to ulceration in healthy individuals, exacerbation of chronic gastrointestinal inflammatory diseases and can lead to cancer...

...A daily intake exceeding the RDA was also found for other key nutrients such as iron. The daily intake of iron was found to be 1874% of the published Korean RDA (18 mg) for supplement users in comparison to 62% RDA for non-supplement users.

In simple iron deficiency anemia, the serum iron is low, the transferrin is high, and therefore the percent transferrin saturation is very low.

On the other hand, in anemia of chronic disease, the body holds iron out of the serum but also produces less transferrin (presumably as part of a response to keep iron away from pathogens that require it for their metabolism). In this case, serum iron is low but the TIBC (that is, the transferrin) is low. So the percent transferrin saturation is normal.

I had my iron tested in November 2007. It was 28 (ref range 40-175); the iron binding capacity 355 (in range); % saturation 8 (ref range 15-50%). I am not anemic, just pretty darned low.

Anemia is a condition where there is a lower than normal number of red blood cells in the blood, usually measured by a decrease in the amount of hemoglobin. Hemoglobin is the oxygen-carrying part of red blood cells. It gives these blood cells their red color

We also absorb less iron during times of inflammation"

In anemia of chronic disease without iron deficiency, ferritin levels should be normal or high, reflecting the fact that iron is stored within cells, and ferritin is being produced as an acute phase reactant but the cells are not releasing their iron. In iron deficiency anemia ferritin should be low.