Anemia is LOW OXYGEN carrying ability by red blood cells. There are over 12 types of anemia with true iron anemia being the least frequently occuring. Iron is an essential nutrient the body is a withholding to protect it from inflammation and microbial overgrowth.
Anemia of Chronic Inflammation is the Evil Twin of Iron Anemia.
Think of it like this: A bunch of children are coming to stay in your house. The risk of something getting broken or damage is high. The children are magnetically drawn to sharp objects. Someone is going to get hurt if sharp objects are left lying around. What do you do? Put them away in a safe place until children leave. Inflammation and microbes are the children. Iron is the sharp object. Your body weighs the risk to benefit option and stores iron in a safe place, the liver, until the inflammation is gone and the microbes under control. It is better to be a little anemic than suffer from the damage from the combined effect of inflammation and microbes gone wild.This makes it appear like you have low iron.
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Iron related Anemia
- Iron Anemia
- Anemia of Chronic Inflammation
- Mistaken for Iron Anemia
- Anemia of Protein Depletion
- Anemia secondary to Liver disease
- Intrinsic Factor Deficiency
- Immune Hemolytic Anemia
Unfortunately, for most (no profession excluded) after the final exam is taken, only iron anemia is remembered. This becomes even more evident when healthcare professionals of stature, i.e. Dr. Oz, fails to discuss the difference between Iron anemia and Anemia of Chronic Inflammation during a nationally syndicated program, especially with so many people suffering from chronic inflammation. In these cases iron supplements promote more free radical production and overgrowth of disease causing bacteria.
So many patients have come into my office taking iron because their doctor recommended it without any lab testing. Coincidentally, they went from bad to worse after starting the iron. But they keep taking it, knowing it is supposed to help them. Before taking iron, you should know what anemia is. Until recently, the available data regarding the adverse effects of dietary supplements has been limited and grossly underreported. We think the paradigm “the more, the better” is wrong.
Anemia meaning “without blood”, is defined as a qualitative or quantitative deficiency of hemoglobin, a molecule inside red blood cells (RBCs). As hemoglobin carries oxygen from the lungs to the tissues, anemia leads to hypoxia (LACK OF OXYGEN) in organs. Since all human cells depend on oxygen for survival, varying degrees of anemia can have a wide range of clinical consequences.
Broadly, causes of anemia may be classified as impaired red blood cell (RBC) production, increased RBC destruction (hemolytic anemias), blood loss and fluid overload (hypervolemia). Several of these may interplay to cause anemia eventually. See Full List
- Impaired production
- Disturbance of proliferation and differentiation of stem cells
- Disturbance of proliferation and maturation of erythroblasts
- Other mechanisms of impaired RBC production
- Increased destruction: Hemolytic anemia
- Extrinsic (extracorpuscular) abnormalities
- Mechanical trauma to red cells
- Blood loss
- Fluid overload
It is not possible to improve adrenal/blood sugar patterns if you are anemic. If you are anemic, your blood cells will not be able to deliver oxygen to the mitochondria for ATP production and become dependent upon glycolysis for energy production. This causes constant fatigue. Glycolysis is an inefficient ATP pathway and will place great demands upon the blood sugar/adrenal stabilizing system. Iron supplementation in the presence of inflammation will increase free radicals enhancing the inflammatory processes.
We know that Dr. Oz recognizes the importance of inflammation as there are 8,640,000 Dr. Oz results doing an Internet search.
Anemia of Chronic Inflammation
Chronic inflammation (also known as chronic systemic inflammation) is an inflammatory immune response of prolonged duration that eventually leads to tissue damage. Chronic inflammation is differentiated from acute inflammation by extended duration, lasting anywhere from a week to an indefinite time frame. The exact nature of chronic inflammation depends on the causative agent and the body’s attempts to ameliorate it.
Anemia of chronic disease, increasingly referred to as “Anemia of Chronic Inflammation”, is a form of anemia seen in chronic illness, e.g. from chronic inflammation, chronic immune activation, autoimmunity or malignancy. New discoveries suggest that the syndrome is likely primarily the result of the body’s production of hepcidin, a master regulator of human iron metabolism.
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Iron is an oxidant as well as a nutrient for probiotic bacteria, as well as invading bacteria and cancer cells. Iron is necessary for bacteria to reproduce. Many probiotic companies put some form of iron in their probiotics to stimulate their growth, i.e. Garden of Life. Excessive iron in certain tissues and cells (iron loading) promotes development of infection, neoplasia, cardiomyopathy, arthropathy, and various endocrine and possibly neurodegenerative disorders. To contain and detoxify the metal, your body has evolved an iron withholding defense system, but the system can be compromised by numerous factors. An array of behavioral, medical, and immunologic methods is in place or in development to strengthen iron withholding.
While no single test is always reliable to distinguish the true causes of disease, there are sometimes some suggestive data:
PURE IRON DEFICIENCY ANEMIA SHOULD IMPROVE MARKEDLY IN RESPONSE TO IRON SUPPLEMENTS, WHILE ANEMIA OF CHRONIC INFLAMMATION WILL NOT. Many will improve initially but the inflammation and microbial overgrowth will soon overwhelm the body’s ability to control the situation. More is not always better.
The number of infectious bacteria whose virulence is enhanced by iron continues to increase. (see list below) To obtain iron, successful pathogens use one or more of four strategies: binding of ferrated siderophilins with extraction of iron at the cell surface; breaking down red blood cells, digestion of hemoglobin, and heme assimilation; use of siderophores that withdraw iron from transferrin; and procurement of intracellular iron.
In response to inflammatory cytokines, several process are put into action to protect the body. In one, the liver produces increased amounts of hepcidin. In another process, an inflammatory hormone – etiocholanolone – levels are increased may be causing symptoms of inflammation, fever, leukocytosis, increased serum C-reactive protein, low iron (hypoferremia), increased IL-1 lymphocyte activation and increased white blood cell activity.
Hepcidin in turn stops ferroportin from releasing iron stores. Inflammatory cytokines also appear to affect other important elements of iron metabolism, including decreasing ferroportin expression, and probably directly blunting erythropoiesis by decreasing the ability of the bone marrow to respond to erythropoietin making your blood test report low iron.
Before the recent discovery of hepcidin and its function in iron metabolism, anemia of chronic inflammation was seen as the result of a complex web of inflammatory changes. In the short term, the overall effect of these changes is likely positive: it allows the body to keep more iron away from bacterial pathogens in the body, while producing more immune cells to fight off infection. Bacteria, like most life forms, depend on iron to live and multiply. However, if inflammation continues, the effect of locking up iron stores is to reduce the ability of the bone marrow to produce red blood cells. These cells require iron for their massive amounts of hemoglobin which allow them to transport oxygen. Iron supplements or probiotic iron used as growth stimulators in probiotics will provide bacteria with a readily available source of iron. There are numerous bacteria species that have an affinity for iron. They will actively seek out and destroy blood cells causing anemia of chronic inflammation.
Small intestinal bacterial overgrowth (SIBO), also termed bacterial overgrowth, is a disorder of excessive bacterial growth in the small intestine. Unlike the colon (or large bowel), which is rich with bacteria, the small bowel usually has eighty percent less bacteria. Patients with bacterial overgrowth typically develop symptoms including acid reflux, nausea, bloating, pain, gas, malnutrition, weight loss and malabsorption which are caused by a number of mechanisms. When bacteria migrate into the upper sections of the small intestine, they are no longer beneficial becoming detrimental to health. SIBO bacteria produce more toxic substances some of which alter hormone elimination.
Increased estrogen tends to have a stimulatory effect on the immune system, while testosterone tends to have suppressive effects. For example, estrogen enhances the secretion of the cytokines IFN-γ, IL-1, and IL-10. Increased etiocholanolone causes a rapid fall in serum iron and a rise in serum ferritin. The effects can last for up to 10 days.[i]
Etiocholanolone, one of the metabolites of the adrenal androgens and testosterone, can cause the above listed symptoms when it exceeds the normal capacity of the liver to transport it or when the ability of the liver to process normal amounts of adrenal androgens and testosterone for elimination through the kidneys is impaired. Certain individuals have episodic bouts of inflammation or fever due to periodic accumulation in the blood of unprocessed Etiocholanolone. Some may describe these episodic bouts as hot flashes.
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[i] Adamson J. The Anemia of Inflammation/Malignancy: Mechanisms and Management. ASH Education Book January 1, 2008 vol. 2008 no. 1 159-165
- Shortness of breath
- Decreased performance at work or school
- Sore and swollen tongue and lips
- Intolerance to cold
Please not the similarity in the symptoms caused by certain bacterial species and iron deficiency:
Pathogenic Bifidobacterium Dentium
- Dental pain alleviated only by loss or extraction of affected tooth.
- Acidification of mouth.
- Caused extensive demineralization of tooth tissues.
- Dental cavities or caries.
- Coronal caries in adults and children.
- Root caries in adults.
- Progressive tooth decay
- Significant alteration in the composition of the commensal microbiota, including bifidobacteria, lactobacilli, Actinomyces and streptococci proliferating.
- High iron affinity and is involved in iron acquisition and adhesion Produce hemolysins that in cooperation with complement causes dissolution of red blood cells.
- Produce an extracellular toxic complex lipopolysaccharide.
- May colonize the skin, pharynx, or gastrointestinal tract.
- Common sites include the urinary tract, lower respiratory tract, biliary tract, and surgical wound sites.
- Availability of iron increases host susceptibility to infection.
Mycoplasma can cause severe anemia. This parasite attaches to the red blood cells and causes damage to the Red Blood Cell (RBC) membrane, which causes it to be destroyed.
- Cause chronic but mild infections.
- Cause immortalization of immune cells
- Night sweats
- Intermittent fevers
- Chronic fatigue
- Skin rashes
- Increased skin sensitivity
- Joint and muscle pain
- Swelling and reduced mobility of joints
- Heart palpitations
- Pain and arrhythmia
- Stomach cramps and regurgitation
- Loss of vision, double vision, and the list can go on.
- Cold agglutinin disease – Exposure to cold may significantly worsen anemia.
- Raynaud’s phenomenon
Sulfate-reducing bacteria (SRB)
Species able to release free sulphate for utilization by sulphate-reducing bacteria:
- Bacteria of the Bacteroides fragilis group
Exposure to low-level concentrations can result in:
- Eye irritation
A sore throat and cough
Shortness of breath
- Fluid in the lungs.
Symptoms that may arise, in typical order of occurrence, include:
- Digestive or bowel complaints such as diarrhea, constipation, gas pains, bloating, or belching.
Foul smelling stool/gas, Pass large amounts of foul smelling gas, Excessive passage of gas
- Nausea, vomiting, loss of appetite and weight loss.
- Enlarged liver and gallbladder.
- Clay or light colored stools.
- Blood clots in the legs.
- Hair loss
Long-term low-level exposure may result in:
- Loss of appetite
- Poor memory
- Offensive breath
- Wake up tired even after 6 or more hours of sleep
- Feel cold-hands, feet all over
- Requires excessive amount of sleep to function properly
- Thinning of hair on scalp, face, or genitals or excessive falling hair
- Mental sluggishness
- Rotten egg odor of hydrogen sulfide
- Discoloration of skin by copper jewelry or coins
- Foul smelling stool
Avoid Sulphate, Sulphite containing foods including but not limited to:
Glucosamine Sulphate, Chondroitin Sulphate, MSM and other sulphate containing supplements.
Avoid Iron Supplement in the presence of inflammation
Iron stimulates free-radical production, probiotic, opportunistic and pathogenic microbial overgrowth and neoplastic (cancer) cells.
Anemia and Autoimmune Thyroid
Anemia was observed in 82% of patients with autoimmune thyroid disease (AITD) and Atrophic body gastritis (ABG) but only in 22% of patients without ABG. In the patients with AITD studied, about one third had ABG, which was diagnosed also in young patients, the presence of anemia, even microcytic, was suggestive of undiagnosed ABG. The increased frequency of chronic anemia in patients with autoimmune thyroid disease (ATD) is essentially due to the presence of concomitant autoimmune gastrointestinal diseases.
Disturbance of proliferation and differentiation of stem cells.
- Pure red cell aplasia
- Aplastic anemia, affecting all kinds of blood cells. Fanconi anemia is a hereditary disorder or defect featuring aplastic anemia and various other abnormalities.
- Anemia of renal failure, by insufficient erythropoietin production
- Anemia of endocrine disorders
Disturbance of proliferation and maturation of erythroblasts
- Pernicious anemia is a form of megaloblastic anemia due to vitamin B12 deficiency dependent on impaired absorption of vitamin B12.
- Anemia of folic acid deficiency. As with vitamin B12, it causes megaloblastic anemia
- Anemia of prematurity, by diminished erythropoietin response to declining hematocrit levels, combined with blood loss from laboratory testing. It generally occurs in premature infants at 2 to 6 weeks of age.
- Iron deficiency anemia, resulting in deficient heme synthesis
- Thalassemias, causing deficient globin synthesis
- Congenital dyserythropoietic anemias, causing ineffective erythropoiesis
- Anemia of renal failure (also causing stem cell dysfunction)
Other mechanisms of impaired RBC production
- Myelophthisic anemia or myelophthisis is a severe type of anemia resulting from the replacement of bone marrow by other materials, such as malignant tumors or granulomas.
- Myelodysplastic syndrome
- Anemia of chronic inflammation
Increased destruction: Hemolytic anemia
Anemias of increased red blood cell destruction are generally classified as hemolytic anemias. These are generally featuring jaundice and elevated LDH levels.
- Intrinsic (intracorpuscular) abnormalities, where there the red blood cells have defects that cause premature destruction. All of these, except paroxysmal nocturnal hemoglobinuria, are hereditary genetic disorders.
- Hereditary spherocytosis is a hereditary defect that results in defects in the RBC cell membrane, causing the erythrocytes to be sequestered and destroyed by the spleen.
- Hereditary elliptocytosis, another defect in membrane skeleton proteins
- Abetalipoproteinemia, causing defects in membrane lipids
- Enzyme deficiencies
- Pyruvate kinase and hexokinase deficiencies, causing defect glycolysis
- Glucose-6-phosphate dehydrogenase deficiency and glutathione synthetase deficiency, causing increased oxidative stress
- Sickle cell anemia
- Hemoglobinopathies causing unstable hemoglobins
- Paroxysmal nocturnal hemoglobinuria
Extrinsic (extracorpuscular) abnormalities
- Warm autoimmune hemolytic anemia is an anemia caused by autoimmune attack against red blood cells, primarily by IgG. It is the most common of the autoimmune hemolytic diseases. It can be idiopathic, that is, without any known cause, drug-associated or secondary to another disease such as systemic lupus erythematosus, or a malignancy, such as chronic lymphocytic leukemia (CLL)
- Cold agglutinin hemolytic anemia caused by Mycoplasma and is primarily mediated by IgM. Raynoud’s Syndrome
- Rh disease, one of the causes of hemolytic disease of the newborn
- Transfusion reaction to blood transfusions
Mechanical trauma to red cells
- Microangiopathic hemolytic anemias, including thrombotic thrombocytopenic purpura and disseminated intravascular coagulation
- Infections, including malaria
- Heart surgery
- Anemia of prematurity from frequent blood sampling for laboratory testing, combined with insufficient RBC production.
- Trauma or surgery, causing acute blood loss
- Gastrointestinal tract lesions, causing a rather chronic blood loss
- Gynecologic disturbances, also generally causing chronic blood loss
Fluid overload (hypervolemia) causes decreased hemoglobin concentration and apparent anemia:
- General causes of hypervolemia include excessive sodium or fluid intake, sodium or water retention and fluid shift into the intravascular space.
- Anemia of pregnancy is anemia that is induced by blood volume expansion experienced in pregnancy
 Table 12-1 in: Mitchell, Richard Sheppard; Kumar, Vinay; Abbas, Abul K.; Fausto, Nelson. Robbins Basic Pathology. Philadelphia: Saunders. ISBN 1-4160-2973-7. 8th edition.
 Weng, CH; Chen JB, Wang J, Wu CC, Yu Y, Lin TH (23). “Surgically Curable Non-Iron Deficiency Microcytic Anemia: Castleman’s Disease.”. Onkologie 34 (8-9): 456-8.
 Cotran, Ramzi S.; Kumar, Vinay; Fausto, Nelson; Nelso Fausto; Robbins, Stanley L.; Abbas, Abul K. (2005). Robbins and Cotran pathologic basis of disease. St. Louis, Mo: Elsevier Saunders. p. 637.
 Berentsen S, Beiske K, Tjønnfjord GE (October 2007). “Primary chronic cold agglutinin disease: An update on pathogenesis, clinical features and therapy”. Hematology 12 (5): 361–70.
 Centanni M, Marignani M, Gargano L, Corleto VD, et al. Atrophic body gastritis in patients with autoimmune thyroid disease: an underdiagnosed association. Arch Intern Med. 1999 Aug 9-23;159(15):1726-30.
 Sibilla R, Santaguida MG, Virili C, Gargano L, Nardo S, et al. Chronic unexplained anaemia in isolated autoimmune thyroid disease or associated with autoimmune related disorders. Clin Endocrinol (Oxf). 2008 Apr;68(4):640-5. Epub 2007 Dec 6.