The Marshall Protocol Study Site > ABOUT THE MARSHALL PROTOCOL > Marshall Protocol FAQs (Required Reading) > My doctor says I'm anemic. What should I do?
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The Marshall Protocol Study Site > ABOUT THE MARSHALL PROTOCOL > Marshall Protocol FAQs (Required Reading) > My doctor says I'm anemic. What should I do? |
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| Moderated by: Dr Trevor Marshall | ||
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Foundation Staff. . 
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My doctor says I'm anemic. What should I do? Anemia is common in Th1 inflammation. It is not due to iron deficiency and will not be helped by iron supplements. In fact, iron supplements are counterproductive because iron will help L-forms multiply. Many physicians are aware of the anemia of chronic disease - or the anemia of infection and inflammation. This is one of the most common syndromes in medicine. If your physician is not aware of this, please share this information with him/her. According to the textbook "An Introduction to Human Disease: Pathology and Pathophysiology Correlations" by Leonard V. Crowley, "Many conditions may depress bone marrow functions. Chronic diseases of all types may impair hematopoiesis and lead to mild or moderate anemia, which is called the anemia of chronic disease... The most common cause of this type of anemia is chronic infection, but other chronic diseases and some malignant tumors may also be responsible." See Diagnosing Anemia GI bleeding A simple outpatient two minute check of your stool for blood would rule out your doctor's concerns pertaining to bleeding into the gut. (Hemoccult test in this country) Anemia of chronic disease pathogenesis A number of bacterial pathogens have developed a mechanism for acquiring iron directly from the (human) host. These bacteria can actually hoard iron for their own use (instead of the human's benefit). Bacteria use several mechanisms to successfuly compete for available iron in the host, and their increased supply of iron may enhance bacterial pathogenicity. The human body has limited defense mechanisms to limit the availability of iron to bacteria, thus blocking their growth. Once this iron-restricted erythropoiesis and the 'anemia of chronic disease' has developed, iron supplementation is not useful. Iron transport and anemia are related to cytokines that are produced in inflammatory and infectious diseases, such as Tumor Necrosis Factor alpha and Interferon Gamma. The cytokines associated with Th1 immune response are sensitive to intracellular iron concentration. The regulation of iron transport by cytokines is a key mechanism in the pathogenesis of anemia of chronic disease. See Iron is required for growth of bacteria In sarcoidosis, granuloma sequester Ferritin and iron, and the low assay is closely tied to the presence of inflammatory granuloma. Serum ferritin may be high in anemia of chronic disease, especially if the liver is involved. One of the potential 'benefits' of the anemia of chronic disease is that bacteria are being starved of the iron essential for their proliferation. Once CWD bacteria are killed off, iron stores will be available for your own body once again. Fatigue from chronic disease is a common symptom and is seen even in patients without anemia. Fatigue is not directly related to anemia. It will gradually resolve as Th1 inflammation resolves on the protocol but it it is often one of the longer-lasting symptoms. See Bacterial iron acquisition systems Testing Hemoglobin, hematocrit and serum ferritin are the most common ways to test for anemia but they do not differentiate between iron deficiency anemia (IDA) and anemia of chronic disease. Normal hemoglobin results vary, but in general are: -Male: 13.8 to 17.2 gm/dL (140-174g/l) -Female: 12.1 to 15.1 gm/dL (123-157g/L) Hematocrit is a blood test that measures the number of red blood cells and the size of red blood cells. It gives a percentage of red blood cells found in whole blood. Most automated cell counters measure the hemoglobin directly, but the hematocrit is calculated. Generally, therefore, it is probably more reliable to base clinical decisions on the hemoglobin concentration. Iron supplements are usually well tolerated by patients so many doctors will not bother to definitively diagnose iron deficiency anemia. They will use iron supplements as a therapeutic probe and retest Hgb and Hct to see it they are effective. Before you agree to taking an iron supplement, talk with your doctor about further testing to determine if you have anemia of chronic disease. To identify iron deficiency anemia, hemoglobin must be measured together with more selective measurements of iron status. This article lists the other tests done when a differential diagnosis is needed. Ask your doctor to test: -serum ferritin. -serum iron -total iron binding capacity (TIBC; an indirect reflection of the transferrin level) -percent transferrin saturation (calculated from the serum iron and the TIBC) -soluble transferrin receptor (sTfR) All of these tests reflect slightly different aspects of internal iron metabolism and give the most complete picture of the iron status of the patient. Serum (soluble) transferrin receptor A new test called serum transferrin receptor (sTfR) is a good way to verify anemia of chronic desease because it is not affected by inflammation. Serum ferritin may be high in anemia of chronic disease, especially if the liver is involved. The normal range for serum transferrin receptor is 3-9 mg/l. The sTfR test should be considered for anemic patients whose differential diagnosis includes iron deficiency and anemia of inflammatory disease. Transferrin receptor values are elevated in iron deficiency anemia (IDA), and in chronic hemolytic anemias.  According to this reference: Anemia of chronic disease and iron deficiency anemia, the most common forms of anemia, are differentiated primarily by estimates of iron status. Standard measures of iron status, such as ferritin, total iron-binding capacity, and serum iron are directly affected by chronic disease. In contrast, soluble transferrin receptor (sTfR) is elevated in iron deficiency but is not appreciably affected by chronic disease. The normal range for serum transferrin receptor is 3-9 mg/l. In summary Anemia of chronic disease equals: -ferritin normal or high -iron low -normal to low soluble transferrin receptor (sTfR) -normal to low total iron-binding capacity (TIBC) Anemia may excerbate due to immunopathology The antibiotics on the Marshall Protocol will treat the underlying disease (bacterial pathogens) and the cytokines associated with infection and inflammation to resolve this anemia. During treatment, however, it is expected that anemia might temporarily worsen during the immune system reaction to antibiotic therapy. It is suggested (male or female) that if your Hgb falls to 11 and/or your Hct falls to 28, you should slow down your immune response by managing all aspects of the MP. Please see My immune system reaction is too strong. What should I do? If you need help with this, please ask a moderator for assistance in your progress report on the website. Recheck your Hgb/Hct in a few weeks to make sure they are going back up. It may take 24-36 months for anemia blood markers to return to normal range. See How long does the MP take? Hgb and Hct are effective tests to monitor anemia of chronic disease. It is not necessary to test Hgb and Hct often. Your doctor will use his/her judgement re the frequency of testing to monitor your anemia. "You are assuming that anemia is a condition whose seriousness is comparable to your Th1 immune disease. It is not. The Th1 disease will kill you. You and Doc need to balance which is the more important issue to focus upon." ~Dr. Marshall There are four different types of tests that measure the body's iron levels and storage.They are called iron level tests, total iron-binding capacity (TIBC) tests, ferritin tests, and transferrin tests. Iron Iron is associated with Th1 immune activity. Macrophages, the Th1 phagocyte, accrete ferritin. Ferrodoxin is also oxidized and reduced when 25-D is converted to 1,25-D. So iron is closely associated with Th1. The iron level test measures the amount of iron in the blood serum that is being carried by a protein (transferrin) in the blood plasma. Serum iron (60-170 mcg/dl) on its own provides no useful information. Serum iron has a diurnal variation that can be as much as 30% within a single individual, it is sensitive to the day's dietary iron intake and is affected by all the confounding diseases listed above. A low serum iron picked up as an incidental finding has a very low specificity for iron deficiency. Serum ferritin The ferritin test measures the level of a protein in the blood that stores iron for later use by the body. Serum ferritin represents the iron stores in the body. Serum ferritin is also an acute phase reactant and will rise rapidly in the face of inflammation. Iron depletion (low serum ferritin) does not prove iron deficiency anemia. We do not know how low is too low for iron stores to go. Your doctor may not be happy until your iron is within the normal range. If you decide to supplement we suggest that you retest frequently to maintain the level at the bottom of the normal range. Male: 12-300 ng/mL Female: 12-150 ng/mL Total iron-binding capacity TIBC is typically measured along with serum iron to evaluate people suspected of having either iron deficiency or iron overload. The iron concentration divided by TIBC gives the transferrin saturation, which is a more useful indicator of iron status than iron or TIBC alone. The TIBC test measures the amount of iron that the blood would carry if the transferrin were fully saturated. Since transferrin is produced by the liver, the TIBC can be used to monitor liver function and nutrition. Transferrin The transferrin test is a direct measurement of transferrin--which is also called siderophilin--levels in the blood. Some laboratories prefer this measurement to the TIBC. The saturation level of the transferrin can be calculated by dividing the serum iron level by the TIBC. It is customary to test for transferrin (instead of TIBC) when evaluating a patient's nutritional status or liver function. Because it is made in the liver, transferrin will be low with liver disease. Transferrin levels also drop when there is not enough protein in the diet, so this test can be used to monitor nutrition. Iron supplements Do not take iron supplements in an effort to increase hemoglobin and and hematocrit. Iron will only help the CWD bacteria multiply. Increasing iron in your diet would also be counterproductive. This article from the CDC's Emerging and Infectious Diseases explains how microbes sequester iron from the host: "Iron Loading and Disease Surveillance" http://www.cdc.gov/ncidod/EID/vol5no3/weinberg.htm Transferrin saturation Transferring saturation (normal 20-50%). As an index of iron transport rather than storage, this measure (calculated from serum iron and TIBC) is an alternative to serum ferritin. However, as it is affected by the same confounding factors it will not add much additional information in iron deficiency if a serum ferritin has already been ordered. A serum transferrin saturation of >55% can be a very useful indication of possible iron overload. On the other hand, if serum ferritin is elevated but transferrin saturation is low, the patient is unlikely to have iron overload. Total Iron Binding Capacity (TIBC) Total iron binding capacity (TIBC) is a blood test that shows if there is too much or too little iron in the blood. This test helps measure the ability of a protein called transferrin to carry iron in the blood. Normal range 240-450 mcg/dl Mean corpuscular volume (MCV) -- measures the size of the red blood cells.Larger or smaller than normal red blood cells may indicate anemia. Ref. Range 80 - 97 Mean corpuscular volume is decreased in anemia of chronic disease. Tracking immunopathology with lab tests -Transient decrease in Hgb and hematocrit are common in the early phases of the MP. My use of lab tests is to help determine pace of therapy......~Greg Blaney, MD When palliation treatment is necessary Blood transfusions If your Hct and Hgb are dangerously low a blood transfusion asap is the standard treatment. A Canadian Critical Care Trial Group study compared “restrictive” Hgb<7) to “liberal” (Hgb<10) transfusion strategies. The “restrictive” strategy was as effective and superior to the “liberal” transfusion strategy among patients less than 55 and without cardiac disease. Patients had an overall greater decrease in mortality and less complications. They concluded that a transfusion threshold of 7 g/dl is safe in critically ill patients, including those with minimal cardiopulmonary disease. Recent recommendations suggest RBC transfusion only in cases with <Hgb and known clinical symptoms. Blood transfusions should not be given unless warranted by dangerously low Hct and Hgb because they carry serious risks. Not listed is also the probable infusion of CWD bacteria with each transfusion. Erythropoiesis-stimulating agents Although they are not without risk and we do not recommend them, Erythropoiesis-Stimulating Agents ((Aranesp, (Epogen and Procrit) may be necessary if Hct and Hgb are extremely low and do not respond quickly to measures to reduce your immune system reaction. ESAs (Procrit and Epogen) do increase red blood cells but they also have serious side effects and we don't know how they might affect the immune system. The decision to treat is based on risk/benefit. Doctors using these drugs are advised "to maintain the lowest hemoglobin level consistent with avoiding the need for transfusions." It isn't necessary to maintain a normal Hgb and Hct while you are recovering on the MP. Members' experiences -My red blood count has risen into the normal range without any kind of iron or vitamin supplemenation. ~NorCalJim in phase 3 You can find personal stories in the topic Anemia and Th1 Disease. Pernicious anemia ................. Last edited on Sun Jul 27th, 2008 02:17 by |
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(filelink) When serum ferritin is high Serum ferritin may be high in chronic inflammation, especially if the liver is involved. Treating that inflammation with the MP, is the answer. Periodic increases in ferritin suggest a good Herx response. This article lists the other tests done when a differential diagnosis is needed. |
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