Hello All, I was just wondering how much additional Iron do you take daily, if you do at all?  I going to have my level checked and was wondering what a normal dose is for us WLS'ers, at this time I take 28 mg a day. Just some thoughts.....

I attempted a very detailed email this am and my laptop crashed w battery dead (our poer is out still since last eve 8pm) email me offlist I will send u stuff from home, its so hard to post as my slow dial up takes forever to load these pages! :-) [email protected]

 

 

DEB

Hi, iron is something that SHOULD NOT BE SUPPLIMENTD UNLESS THERE IS A DOCUMENTED LAB DEFICIENCY. I became anemic after plastics using ferrous gluconate 3x ay each tab salt wt is 300mg or 35mg elemental each now I need one a day for life with vit c 500mg Read on for what not to take iron with, even though I have a mirena iud and don’t bleed at all I am still anemic.had it 3 yrs..

No normal dose is based on labs and what your body will absorb some need only oral iron others need IZM others infusions some not at all ~35%wlsers become anemic….

http://www.merck.com/mmpe/sec01/ch005/ch005f.html

Toxicity: Iron may accumulate in the body when a person receives iron therapy in excessive amounts or for too long, is given repeated blood transfusions, has chronic alcoholism, or takes an overdose of iron. Excess iron is toxic, causing vomiting, diarrhea, and damage to the intestine and other organs. Toxicity can also result from iron overload disease (hemochromatosis—see Iron Overload), a potentially fatal but easily treatable genetic disorder in which too much iron is absorbed. Hemochromatosis affects > 1 million Americans.

 

 

 Typically the labs that would indicate this are: Anemia

 

http://labtestsonline.org/understanding/conditions/anemia.ht ml

Anemia occurs when the amount of hemoglobin (found in the red blood cells) drops below normal. Hemoglobin is necessary for the transportation of oxygen throughout the body. There are many different types of anemia, but we will limit this page to the most common ones.

 

Iron and Vitamin Deficiencies Iron deficiency anemia is the most common of the anemias and is usually due to bleeding. In women, iron deficiency may be due to heavy menstrual periods, but in older women and in men, the bleeding is usually from disease of the intestines. In children and in pregnant women, the body needs more iron, and iron deficiency may be due simply to not eating enough iron in the diet. Iron deficiency may also result from some extreme diets. Treatment of iron deficiency usually involves iron supplements. In older women and in men, there is usually also some further testing to determine why the person is iron deficient.

 

Pregnant and nursing women frequently develop this deficiency since the baby requires large amounts of iron for growth. Lack of iron can lead to low birth weight babies and premature delivery. Pre-pregnant and pregnant women are routinely given iron supplements to prevent these complications. Newborns who are nursing from deficient mothers tend to have iron deficiency anemia as well.

 

Blood tests may show a normal or low hemoglobin, decreased iron, ferritin, and all red blood cell indices. The total iron-binding capacity (TIBC) or transferrin will be increased. The ferritin test is considered to be the most specific for identifying iron deficiency anemia.

 

Vitamin B12 deficiency is less common than iron deficiency and is usually not due to dietary deficiency of vitamin B12. The most common cause is a disease called pernicious anemia, in which the body stops making a substance (called “intrinsic factor”) that is needed to absorb vitamin B12 from the diet. Vitamin B12 deficiency can also cause nerve problems, often causing numbness and tingling that start first in the hands and feet. Hemoglobin is low, but red blood cell indices are usually increased.

 

Folic acid deficiencycan cause the same pattern of changes in hemoglobin and the red cell indices as does vitamin B12 deficiency. Folic acid is found in many foods, especially in green, leafy vegetables. Folic acid is also added to most grain products in the United States so that deficiency in folic acid is rarely seen in the U.S. today. During pregnancy, however, there is an increased need for folic acid so deficiency can develop during this time. This is especially dangerous because deficiency in folic acid can cause problems in the development of the brain and spinal cord of the baby. Pregnant women usually need folic acid supplements.

 

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Ferritin

http://labtestsonline.org/understanding/analytes/ferritin/te st.html

 

 

 

How is it used?

 

The ferritin test is ordered to see how much iron your body has stored for future use. The test is done, usually with an iron test and the TIBC, to learn about iron levels in your blood.

 

What does the test result mean?

 

Ferritin levels are low in chronic iron deficiency and or if your body proteins are severely depleted, as in some cases of malnutrition.

 

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Serum Iron

 

http://labtestsonline.org/understanding/analytes/serum_iron/ test.html

 

How is it used?

 

The iron test is used to measure the amount of iron that is carried by transferrin, which transports iron from the gut to cells that use iron. In persons with anemia, the iron test can help to tell whether it is due to iron deficiency. It can also help to recognize when anemia is due to a chronic illness. The direct iron test can be used as a screening test for hereditary hemochromatosis, along with the transferrin saturation test. The College of American Pathologists recommends screening for hemochromacytosis in all people over age 20, because of the low cost of diagnosis and treatment if caught early. Other organizations have not yet recommended screening, because it is not yet possible to tell which persons who have the abnormal genes will never develop symptoms and which will develop organ damage. A number of studies are currently under way to develop a strategy to determine when and how to screen people.

 

What does the test result mean?

 

A low iron is usually due to iron deficiency, especially if transferrin or TIBC is high. With chronic diseases, low iron occurs with low transferrin or TIBC. High levels of serum iron can occur as the result of many blood transfusions, iron injections into muscle, lead poisoning, liver disease, or kidney disease. Hemochromatosis is the most common cause of high iron.

 

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TIBC & Transferrin

 

http://labtestsonline.org/understanding/analytes/tibc/test.h tml

 

How is it used?

 

TIBC (or transferrin) is typically used along with serum iron to evaluate persons suspected of having too much or too little iron. Usually, about one third of the transferrin measured is being used to transport iron. In iron deficiency, iron is low, but TIBC is increased. In iron overload, such as in hemochromatosis, iron will be high and TIBC will be low or normal. Because transferrin is made in the liver, TIBC and transferrin will also be low with liver disease. Transferrin levels fall relatively rapidly when there is not enough protein in the diet, and so can also be used to monitor nutrition.

 

What does the test result mean?

 

High TIBC usually indicates iron deficiency. A low TIBC may occur if you have hemochromatosis (too much stored iron), anemia caused by infections and chronic diseases, malnutrition, cirrhosis, or nephrotic syndrome (a kidney disease that causes loss of protein in urine).

 

CBC  http://labtestsonline.org/understanding/analytes/cbc/test.html

 

How is it used?

 

The CBC is used as a broad screening test to check for such disorders as anemia (decrease in red blood cells or hemoglobin), infection, and many other diseases. It is actually a panel of tests that examine different parts of the blood. Results from the following tests provide the broadest picture of your health:  some important ones for anemia are:

 

• Red blood cell (RBC) count is a count of the actual number of red blood cells per volume of blood. Both increases and decreases can point to abnormal conditions. Depending on the laboratory's report forms, red blood cells are reported as millions in a microliter of blood (4,250,000/µL or 4.25x106/µL) or as millions in a liter of blood (4.25x1012/L).

   

• Hemoglobin measures the amount of oxygen-carrying protein in the blood

   

• Hematocrit measures the amount of space red blood cells take up in the blood. It is reported as a percentage. 

   

 

 

 

 

How a body absorbs iron is individual, good thing that there are many forms of it out there (things like ferrous gluconate, fumarate, polysaccharide iron, chelated etc) *Most feel we should avoid ferrous sulfate form due to HARSHNESS on pouch and constipation it causes, so it is readily available OTC read labels carefully ok!*Some need one form, others mix 2 forms, some need transfusions, iron injections etc...Can't say what will work for you or dose u will need, work with provider to monitor labs/symptoms....until u seemingly get the right mix.

 

***IRON deficiency is VERY common post WLS men and women, but iron is also something to not fool with too much can be harmful/toxic...So please consider all supplementation with help of labs/provider ok!

 

I was not anemi****il after my plastics (LBL/breast aug) 1.5 yrs post RNY, now i take ferrous gluconate 300mg (salt weight) ~35mg elemental iron in that w/ vit c 500mg once a day to keep everything stable! (iron/ferritin/TIBC/%sat & H&H). I am a Lap proxie 100cm bypassed....

 

 

 

 

 

There is no one size absorbs l iron so no one can say we should take x amount of iron, each form has a different elemental amount per salt weight….

 

 

 

(PDR)

 

 

 

Ferrous sulfate tablets 325 mg dried ferrous sulfate iron = 60 mg elemental iron

 

 

 

Each FEOSOL carbonyl iron caplet delivers 45 mg of pure elemental iron, the same amount of elemental iron contained in the 225 mg ferrous sulfate capsule.

 

 

 

NIFEREX (polysaccharide-iron complex) Film Coated Tablets contain 150 mg elemental iron

 

 

 

Ferrous Gluconate 300mg = 35mg elemental iron

 

 

Iron is mainly absorbed in the duodenum and upper jejunum, which is bypassed in all proxies and distals....this is why the risk! *and many can not take the red meats the may of preop...

http://www-medlib.med.utah.edu/WebPath/TUTORIAL/IRON/IRON.ht ml

for all u wanted to know on iron metabolism etc!

 

 

 

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Who is likely to be deficient?

Vegetarians eat less iron than non-vegetarians, and the iron they eat is somewhat less absorbable. As a result, vegetarians are more likely to have reduced iron stores.¹ However, iron deficiency is not usually caused by a lack of iron in the diet alone. An underlying cause, such as iron loss in menstrual blood, often exists.

Pregnant women, marathon runners, people who take aspirin, and those who have parasitic infections, hemorrhoids, ulcers, ulcerative colitis, Crohn’s disease, gastrointestinal cancers, or other conditions that cause blood loss or malabsorption are likely to become deficient.

Infants living in inner city areas may be at increased risk of iron-deficiency anemia² and suffer more often from developmental delays as a result.^{3 4} Supplementation of infant formula with iron up to 18 months of age in inner city infants has been shown to prevent iron-deficiency anemia and to reduce the decline in mental development seen in such infants in some,⁵ but not all,⁶ studies.

Breath-holding spells are a common problem affecting about 27% of healthy children.⁷ These spells have been associated with iron-deficiency anemia,⁸ and several studies have reported improvement of breath-holding spells with iron supplementation.^{9 10 11 12}

People who fit into one of these groups, even pregnant women, shouldn’t automatically take iron supplements. Fatigue, the first symptom of iron deficiency, can be caused by many other things. A doctor should assess the need for iron supplements, since taking iron when it isn’t needed does no good and may do some harm.

Which forms of supplemental iron are best?

All iron supplements are not the same. Ferrous iron (e.g. ferrous sulfate) is much better absorbed than ferric iron (e.g. ferric citrate).^{13 14} The most common form of iron supplement is ferrous sulfate, but it is known to produce intestinal side effects (such as constipation, nausea, and bloating) in many users.¹⁵ Some forms of ferrous sulfate are enteric-coated to delay tablet dissolving and prevent some side effects,¹⁶ but enteric-coated iron may not absorb as well as iron from standard supplements.^{17 18 19} Other forms of iron supplements, such as ferrous fumarate,^{20 21} ferrous gluconate,²² heme iron concentrate,^{23 24 25 26} and iron glycine amino acid chelate^{27 28} are readily absorbed and less likely to cause intestinal side effects.

How much is usually taken?

If a doctor diagnoses iron deficiency, iron supplementation is essential. To treat iron deficiency, a common recommended amount for an adult is 100 mg per day; that amount is usually reduced after the deficiency is corrected. When iron deficiency is diagnosed, the doctor must also determine the cause. Usually it’s not serious (such as normal menstrual blood loss or blood donation****asionally, however, iron deficiency signals ulcers or even colon cancer.

Some premenopausal women become marginally iron deficient unless they supplement with iron. However, the 18 mg of iron present in many multivitamin-mineral supplements is often adequate to prevent deficiency. A doctor should be consulted to determine the amount of iron that is needed.

Are there any side effects or interactions?

Iron (ferrous sulfate) is the leading cause of accidental poisonings in children.^{29 30 31} The incidence of iron poisonings in young children increased dramatically in 1986. Many of these children obtained the iron from a child-resistant container opened by themselves or another child, or left open or improperly closed by an adult.³² Deaths in children have occurred from ingesting as little as 200 mg to as much as 5.85 grams of iron.³³ Keep iron-containing supplements out of a child’s reach.

Hemochromatosis, hemosiderosis, polycythemia, and iron-loading anemias (such as thalassemia and sickle cell anemia) are conditions involving excessive storage of iron. Supplementing iron can be quite dangerous for people with these diseases.

Supplemental amounts required to overcome iron deficiency can cause constipation. Sometimes switching the form of iron (see “Which forms of supplemental iron are best?” above), getting more exercise, or treating the constipation with fiber and fluids is helpful, though fiber can reduce iron absorption (see below). Sometimes the amount of iron must be reduced if constipation occurs.

Some researchers have linked excess iron levels to diabetes,³⁴ cancer,³⁵ increased risk of infection,³⁶ systemic lupus erythematosus (SLE),³⁷ exacerbation of rheumatoid arthritis,³⁸ and Huntington’s disease.³⁹ The greatest concern has surrounded the possibility that excess storage of iron in the body increases the risk of heart disease.^{40 41 42} Two analyses of published studies came to different conclusions about whether iron could increase heart disease risk.^{43 44} One trial has suggested that such a link may exist, but only in some people (possibly smokers or those with elevated cholesterol levels).⁴⁵ The link between excess iron and any of the diseases mentioned earlier in this paragraph has not been definitively proven. Nonetheless, too much iron causes free radical damage, which can, in theory, promote or exacerbate most of these diseases. People who are not iron deficient should generally not take iron supplements.

Patients on kidney dialysis who are given injections of iron frequently experience “oxidative stress”. This is because iron is a pro-oxidant, meaning that it interacts with oxygen molecules in ways that can damage tissues. These adverse effects of iron therapy may be counteracted by supplementation with vitamin E.⁴⁶

Supplementation with iron, or iron and zinc, has been found to improve vitamin A status among children at high risk for deficiency of the three nutrients. ⁴⁷

People with hepatitis C who have failed to respond to interferon therapy have been found to have higher amounts of iron within the liver. Moreover, reduction of iron levels by drawing blood has been shown to decrease liver injury caused by hepatitis C.⁴⁸ Therefore, people with hepatitis C should avoid iron supplements.

In some people, particularly those with diabetes, insulin resistance syndrome, or liver disease, a genetic susceptibility to iron overload has been reported.⁴⁹

Many foods, beverages, and supplements have been shown to affect the absorption of iron.⁵⁰

Foods, beverages and supplements that interfere with iron absorption include

·         Green tea (Camellia sinensis).^{51 52 53 54} This effect may be desirable for people with iron overload diseases, such as hemochromatosis. The inhibitory effect of green tea on iron absorption was 26% in one study.⁵⁵

·         Coffee (Coffea arabica, C. robusta).^{56 57 58}

·         Red wine, particularly the polyphenol component (also found in tea).^{59 60} Since wine is also a dietary source of iron, it is not clear whether drinking red wine would lead to a deficiency of iron.

·         Phytate (phytic acid), found in unleavened wheat products such as matzoh, pita, and some rye crackers; in wheat germ, oats, nuts, cacao powder, vanilla extract, beans, and many other foods, and in IP-6 supplements.^{61 62 63}

·         Whole wheat bran, independent of its phytate content, has been shown to inhibit iron absorption.⁶⁴

·         Calcium from food and supplements interferes with heme-iron absorption.^{65 66}

·         Soy protein.^{67 68}

·         Eggs.^{69 70}

Foods and supplements that increase iron absorption include

·         Meat, poultry, and fish.^{71 72 73 74 75}

Although vitamin C increases iron absorption,^{76 77 78 79} the effect is relatively minor.⁸⁰

Taking vitamin A with iron helps treat iron deficiency, since vitamin A improves the absorption and/or utilization of iron.^{81 82}

Although soy protein has been shown to decrease iron absorption (see above), certain soy-containing foods (e.g. tofu, miso, tempeh) have significantly improved iron absorption.⁸³ Some soy sauces may also enhance iron absorption.⁸⁴

Alcohol, but not red wine, has been reported to increase the absorption of ferric, but not ferrous, iron.^{85 86}

Iron has been reported to potentially interfere with manganese absorption. In one trial, women with high iron status had relatively poor absorption of manganese.⁸⁷ In another trial studying manganese/iron interactions in women, increased intake of “non-heme iron”—the kind of iron found in most supplements—decreased manganese status.⁸⁸ These interactions suggest that taking multiminerals that include manganese may protect against manganese deficiencies that might otherwise be triggered by taking isolated iron supplements.

Are there any drug interactions? Certain medicines may interact with iron. Refer to drug interactions for a list of those medicines.

References

1. Sullivan JL. Stored iron and ischemic heart disease. Circulation 1992;86:1036 [editorial].

2. Pollitt E. Poverty and child development: relevance of research in developing countries to the United States. Child Dev 1994;65(2 Spec No):283–95.

3. Hurtado EK, Claussen AH, Scott KG. Early childhood anemia and mild or moderate mental retardation. Am J Clin Nutr 1999;69:115–9.

4. Roncagliolo M, Garrido M, Walter T, et al. Evidence of altered central nervous system development in infants with iron deficiency anemia at 6 mo: delayed maturation of auditory brainstem responses. Am J Clin Nutr 1998;68:683–90.

5. Williams J, Wolff A, Daly A, et al. Iron supplemented formula milk related to reduction in psychomotor decline in infants from inner city areas: randomised study. BMJ 1999;318:693–7

6. Morley R, Abbott R, Fairweather-Tait S, et al. Iron fortified follow on formula from 9 to 18 months improves iron status but not development or growth: a randomised trial. Arch Dis Child 1999;81:247–52.

7. Bridge EM, Livingston S, Tietze C. Breath-holding spells: their relationship to syncope, convulsions and other phenomena. J Pediatr 1943;23:539–61.

8. Holowach J, Thurston DL. Breath-holding spells and anemia. N Engl J Med 1963;268:21–3.

9. Bhatia MS, Singhal PK, Dhar NK, et al. Breath holding spells: an analysis of 50 cases. Indian Pediatr 1990;27:1073–9.

10. Colina KF, Abelson HT. Resolution of breath-holding spells with treatment of concomitant anemia. J Pediatr 1995;126:395–7.

11. Daoud AS, Batieha A, al-Sheyyab M, et al. Effectiveness of iron therapy on breath-holding spells. J Pediatr 1997;130:547–50.

12. Mocan H, Yildiran A, Orhan F, Erduran E. Breath holding spells in 91 children and response to treatment with iron. Arch Dis Child 1999;81:261–2.

13. Dietzfelbinger H. Bioavailability of bi- and trivalent oral iron preparations. Investigations of iron absorption by postabsorption serum iron concentrations curves. Arzneimittelforschung 1987;37:107–12 [review].

14. Davidsson L, Kastenmayer P, Szajewska H, et al. Iron bioavailability in infants from an infant cereal fortified with ferric pyrophosphate or ferrous fumarate.Am J Clin Nutr 2000;71:1597–602.

15. Hansen CM. Oral iron supplements. Am Pharm 1994 Mar;NS34:66–71 [review].

16. Simmons WK, Cook JD, Bingham KC, et al. Evaluation of a gastric delivery system for iron supplementation in pregnancy. Am J Clin Nutr 1993;58:622–6.

17. Ricketts CD. Iron bioavailability from controlled-release and conventional iron supplements. J Appl Nutr 1993;45:13–19.

18. Rudinskas L, Paton TW, Walker SE. Poor clinical response to enteric-coated iron preparations. Can Med Assoc J 1989;141:565–6.

19. Walker SE, Paton TW, Cowan DH, et al. Bioavailability of iron in oral ferrous sulfate preparations in healthy volunteers. Can Med Assoc J 1989;141:543–7.

20. Bender-Gotze C. Therapy of juvenile iron deficiency with bivalent iron dragees (Fe2-fumarate, succinate, sulfate). Controlled double-blind study. Fortschr Med 1980;98:590–3 [in German].

21. Hurrell RF, Furniss DE, Burri J, et al. Iron fortification of infant cereals: a proposal for the use of ferrous fumarate or ferrous succinate. Am J Clin Nutr 1989;49:1274–82.

22. Casparis D, Del Carlo P, Branconi F, et al. Effectiveness and tolerability of oral liquid ferrous gluconate in iron-deficiency anemia in pregnancy and in the immediate post-partum period: comparison with other liquid or solid formulations containing bivalent or trivalent iron. Minerva Ginecol 1996;48:511–8 [in Italian].

23. Frykman E, Bystrom M, Jansson U, et al. Side effects of iron supplements in blood donors: superior tolerance of heme iron. J Lab Clin Med 1994;123:561–4.

24. Martinez C, Fox T, Eagles J, Fairweather-Tait S. Evaluation of iron bioavailability in infant weaning foods fortified with haem concentrate. J Pediatr Gastroenterol Nutr 1998;27:419–24.

25. Hertrampf E, Olivares M, Pizarro F, et al. Haemoglobin fortified cereal: a source of available iron to breast-fed infants. Eur J Clin Nutr. 1990;44:793–8.

26. Calvo E, Hertrampf E, de Pablo S, et al. Haemoglobin-fortified cereal: an alternative weaning food with high iron bioavailability. Eur J Clin Nutr 1989;43:237–43 [review].

27. Fox TE, Eagles J, Fairweather-Tait SJ. Bioavailability of iron glycine as a fortificant in infant foods. Am J Clin Nutr 1998;67:664–8.

28. Pineda O, Ashmead HD, Perez JM, Lemus C. Effectiveness of iron amino acid chelate on the treatment of iron deficiency anemia in adolescents. J Appl Nutr 1994;46:2–13.

29. FDA Medical Bulletin, U.S. Government Printing Office, document number 386–942/00002; February 6, 1995.

30. Nightingale SL. Action to prevent accidental iron poisoning in children. JAMA 1997;27:1343.

31. Krezenlok EP, Hoff JV. Accidental iron poisoning. A problem of marketing and labeling. Pediatrics 1979;63:591–6.

32. Morris CC. Pediatric iron poisonings in the United States. South Med J 2000;93:352–8.

33. Mills KC, Curry SC. Acute iron poisoning. Emerg Med Clin N Am 1994;12;397–413.

34. Cutler P. Deferoxamine therapy in high-ferritin diabetes. Diabetes 1989;38:1207–10.

35. Stevens RG, Graubard BI, Micozzi MS, et al. Moderate elevation of body iron level and increased risk of cancer occurrence and death. Int J Cancer 1994;56:364–9.

36. Weinberg ED. Iron withholding: a defense against infection and neoplasia. Am J Physiol 1984;64:65–102.

37. Oh VMS. Iron dextran and systemic lupus erythematosus. Br Med J 1992;305:1000 [letter].

38. Dabbagh AJ, Trenam CW, Morris CJ, Blake DR. Iron in joint inflammation. Ann Rheum Dis 1993;52:67–73.

39. Bartzokis G, *******s J, Perlman S, et al. Increased basal ganglia iron levels in Huntington disease. Arch Neurol 1999;56:569–74.

40. Salonen JT, Nyyssonen K, Korpela H, et al. High stored iron levels associated with excess risk of myocardial infarction in western Finnish men. Circulation 1992;86:803–11.

41. Kechl S, Willeit J, Egger G, et al. Body iron stores and the risk of carotid atherosclerosis. Circulation 1997;96:3300–7.

42. Tzonou A, Lagiou P, Trichopoulou A, et al. Dietary iron and coronary heart disease risk: a study from Greece. Am J Epidemiol 1998;147:161–6.

43. Danesh J, Appleby P. Coronary heart disease and iron status. Meta-analyses of prospective studies. Circulation