Dr. Leclair on iron defficiency (tomorrow at 9:00 AM)
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Memo To Me
Apr 1, 2021, 8:00:36 AM4/1/21
to MPDSU...@listserv.icors.org
From: Susan Leclair <SLec...@UMASSD.EDU
Subject: Re: patti's iron deficiency
What did he say? Here is how one becomes iron deficient.
1. Iron must be taken in from food or supplements. If your diet is low in iron, you can become deficient simply from that. Food rich in iron AND contains iron that is easily absorbed are red meats. Other food can be rich in iron (spinach for example) but the compound in which the iron is incorporated makes it much harder to separate the iron from the compound and make it available for absorption. thus you have to eat a whole lot more of it to get the same amount of iron as a piece of red meat.
2. Iron is ingested (most often as the ferric form) and altered to the ferrous form by stomach acid. People who use antacids or acid inhibitors (Nexium, Prisolsec, etc.) might not produce adequate acid to do the job and the iron will no be absorbed. Supplements are frequently the ferrous form to lessen this problem.
3. Certain foods will influence the acidity issue. Iron is "encouraged" to be absorbed if taken with orange (or other citrus) juice, wine, beer, etc. and "discouraged" in the presence of milk, soda, coffee or tea.
4. Iron is absorbed by the duodenum (first part of the small intestine). Anytime you have damage to that area (simple upsets to surgical excision to malignancy), the iron will not be absorbed as efficiently.
5. Once absorbed it must be bound to transferrin or it will be excreted via the kidneys and GI tract. Transferrin is made by the liver but it can also be stored/secreted/possibly a small amount made by the white blood cell - monocyte or its older brother, the macrophage. so, deficiencies can happen if your liver is not making transferrin or if the monocytes/macrophages are not making it available.
6. Transferrin brings the iron to the bone marrow where it is taken up by a subset of macrophages sometimes called the nurse cells. In the regular world, the developing red cells blend their membranes with the macrophage and leach the iron from the macrophage as they make hemoglobin. This process begins before hemoglobin is made (since you can't make hemoglobin without the iron) so it is seen in immature red cells. True, if there is a strong inflammatory response, the macrophages will not allow red cells to get the iron and both transferrin and iron are used in inflammation and that apparently has a greater priority than hemoglobin production. If this is the situation, then no amount of additional iron will ever be made available to the developing red cells as these cells will preferentially move it into the inflammatory process. There are tons of articles describing this situation in patients who are anemic due to end stage renal disease, rheumatoid arthritis and other chronic inflammatory conditions. Iron supplement is contra-indicated in many of those situations unless used with EPO.
7. Once iron makes it into the developing red cell, it is incorporated into hemoglobin. That will not happen if the cell's DNA is missing the genes for making some/all
\\\\ To post or reply, email to: MPDSU...@LISTSERV.ICORS.ORG ////
Subject: Re: patti's iron deficiency
What did he say? Here is how one becomes iron deficient.
1. Iron must be taken in from food or supplements. If your diet is low in iron, you can become deficient simply from that. Food rich in iron AND contains iron that is easily absorbed are red meats. Other food can be rich in iron (spinach for example) but the compound in which the iron is incorporated makes it much harder to separate the iron from the compound and make it available for absorption. thus you have to eat a whole lot more of it to get the same amount of iron as a piece of red meat.
2. Iron is ingested (most often as the ferric form) and altered to the ferrous form by stomach acid. People who use antacids or acid inhibitors (Nexium, Prisolsec, etc.) might not produce adequate acid to do the job and the iron will no be absorbed. Supplements are frequently the ferrous form to lessen this problem.
3. Certain foods will influence the acidity issue. Iron is "encouraged" to be absorbed if taken with orange (or other citrus) juice, wine, beer, etc. and "discouraged" in the presence of milk, soda, coffee or tea.
4. Iron is absorbed by the duodenum (first part of the small intestine). Anytime you have damage to that area (simple upsets to surgical excision to malignancy), the iron will not be absorbed as efficiently.
5. Once absorbed it must be bound to transferrin or it will be excreted via the kidneys and GI tract. Transferrin is made by the liver but it can also be stored/secreted/possibly a small amount made by the white blood cell - monocyte or its older brother, the macrophage. so, deficiencies can happen if your liver is not making transferrin or if the monocytes/macrophages are not making it available.
6. Transferrin brings the iron to the bone marrow where it is taken up by a subset of macrophages sometimes called the nurse cells. In the regular world, the developing red cells blend their membranes with the macrophage and leach the iron from the macrophage as they make hemoglobin. This process begins before hemoglobin is made (since you can't make hemoglobin without the iron) so it is seen in immature red cells. True, if there is a strong inflammatory response, the macrophages will not allow red cells to get the iron and both transferrin and iron are used in inflammation and that apparently has a greater priority than hemoglobin production. If this is the situation, then no amount of additional iron will ever be made available to the developing red cells as these cells will preferentially move it into the inflammatory process. There are tons of articles describing this situation in patients who are anemic due to end stage renal disease, rheumatoid arthritis and other chronic inflammatory conditions. Iron supplement is contra-indicated in many of those situations unless used with EPO.
7. Once iron makes it into the developing red cell, it is incorporated into hemoglobin. That will not happen if the cell's DNA is missing the genes for making some/all
\\\\ To post or reply, email to: MPDSU...@LISTSERV.ICORS.ORG ////
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