Anemia

Anemia is common in Th1 inflammationThe complex biological response of vascular tissues to harmful stimuli such as pathogens or damaged cells. It is a protective attempt by the organism to remove the injurious stimuli as well as initiate the healing process for the tissue.. 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-formsDifficult-to-culture bacteria that lack a cell wall and are not detectable by traditional culturing processes. Sometimes referred to as cell wall deficient bacteria. multiply.

Many physicians are aware of the anemia of chronic disease, also called the anemia of infection and inflammationThe complex biological response of vascular tissues to harmful stimuli such as pathogens or damaged cells. It is a protective attempt by the organism to remove the injurious stimuli as well as initiate the healing process for the tissue..¹ This is one of the most common syndromes in medicine.² 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,³ “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.”

A simple outpatient two minute check of your stool for blood would rule out your doctor's concerns pertaining to bleeding into the gut.⁴

A number of bacterial pathogens have developed a mechanism for acquiring iron directly from the (human) host.⁵ These bacteria can actually hoard iron for their own use (instead of the human's benefit). Bacteria use several mechanisms to successfully compete for available iron in the host,⁶ and their increased supply of iron may enhance bacterial pathogenicity.⁷

The human body has limited defense mechanisms to limit the availability of iron to bacteria,⁸ 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 cytokinesAny of various protein molecules secreted by cells of the immune system that serve to regulate the immune system. that are produced in inflammatory and infectious diseases, such as Tumor Necrosis Factor alpha⁹ and Interferon Gamma¹⁰. The cytokines associated with Th1 immune response are sensitive to intracellular iron concentration.¹¹ The regulation of iron transport by cytokines is a key mechanism in the pathogenesis of anemia of chronic disease.^12,13

In sarcoidosis, granuloma sequester Ferritin and iron, and the low assay is closely tied to the presence of inflammatory granuloma.¹⁴ Serum ferritin may be high in anemia of chronic disease, especially if the liver is involved.^15,16

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.

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

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:

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 probeA brief trial of the Marshall Protocol to see if it will generate an immunopathological response. The "gold standard" for testing whether a patient is a good candidate for the MP. 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. When a differential diagnosis is needed, ask your doctor to test:

• serum ferritin
• serum iron
• total iron binding capacity (TIBC)
• percent transferrin saturation
• 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.

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.

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 immunopathologyA temporary increase in disease symptoms experienced by Marshall Protocol patients that results from the release of cytokines and endotoxins as disease-causing bacteria are killed.

The antibiotics on the Marshall ProtocolA curative medical treatment for chronic inflammatory disease. Based on the Marshall Pathogenesis. 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.

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.

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

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.

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.

My red blood count has risen into the normal range without any kind of iron or vitamin supplemenation.

NorCalJim in phase 3

When I was diagnosed with hypothyroidism (from Hashimoto's thyroiditis) I had iron-deficiency anaemia. Doctor ordered me to take iron supplements for a month before he even gave me any thyroxine. BIG mistake. (Not his fault, but had we only known about the MP…) My iron levels came up, yes, I guess because I was ingesting enough to feed myself and all those iron-hungry bacteria! The awful part was I felt more fatigued than ever before and my arthritic joints hurt more than ever before. I was depressed, in pain and had to give up my work as a massage therapist after 25 years.

Once I started thyroxine my life turned around, as I got most of my energy back and my thinning hair started growing back - but my arthritis was as bad as ever.

Fast forward 1 year - I found the MP and began phase one. Within days of starting mino I began to experience a metallic taste in my mouth. Could that metallic taste be … metal? Can't prove it, but my ferritin levels shot through the roof! You can read my phase 1 posts on my thread: http://www.marshallprotocol.com/forum20/5902-1.html

I reckon all those iron-sequestering CWD monsters were dying and giving up all the iron back into my bloodstream. After a couple of months, my ferritin levels came down to normal again and the metallic taste went away at the same time.

So there you have it.

Claudia, MarshallProtocol.com