Decoding iron deficiency

Question: What are the possible causes for not absorbing iron and the resulting low-iron blood? My doctor said she didn’t know and that Western medicine doesn’t address the question; it only attempts to replace the missing iron with prescription iron.

I am currently taking that prescription and my iron levels are very, very slowly responding. I feel I may be missing an important angle on this rather debilitating problem. My doctor says that 85 percent of her patients are low iron. Why are we not asking WHY? (more…)

Naturally avoid and correct dangerous anemia

Anemia is a blood condition in which the number and/or size of the red blood cells is reduced. Because red blood cells move oxygen from your lungs to the tissues, any decrease in size or amount limits how much oxygen is transported. Fortunately, anemia can usually be corrected through proper diet and/or supplementation.

There are 3 different types of nutritional anemia: iron, B-12, and folate. Common symptoms of anemia include weakness, tiredness, poor concentration skills, pale skin, mild depression, and an increased risk of infection.

Iron-deficiency Anemia

Telomere Length in Severe Aplastic Anemia

Anemia is one of the most common clinical problems seen in the elderly. There is a progressive decrease in bone marrow reserve with age and a decrease in hormonal response to hematologic stress. Anemia has been found to increase the risk of non-vertebral fractures. One major factor that is often overlooked that may contribute to the presence of anemia in the older population is nutritional status. While rarely encountered in affluent elderly communities, in lower socioeconomic circumstances where other dietary deficiencies are found, anemia is a much more frequent occurrence. The principle reason for inadequate nutrition status in the elderly is poor dentition.

A telomere is a region of repetitive DNA at the end of a chromosome, which protects the end of the chromosome from deterioration. Telomeres are extensions of the linear, double-stranded DNA molecules of which chromosomes are composed, and are found at each end of both of the chromosomal strands. Thus, one chromosome will have four telomeric tips. In humans, the forty-six chromosomes are tipped with ninety-two telomeric ends. Shorter (systemic) telomere length has been suggested as an independent risk factor for cardiovascular disease. The origin of this association is unclear and several models have been proposed, particularly attributing the biomarker value to a genetic predisposition in subjects with shorter telomeres, to an effect of inflammation and oxidative stress or to a combination of both.

A recent study published in JAMA researched the relationship between telomere length and clinical outcomes in severe aplastic anemia. The study involved 183 patients with severe aplastic anemia who had been treated at the National Institutes of Health from 2000 to 2008. The results were measured by hematologic response, relapse, clonal evolution and survival. Researchers found hematologic response and telomere length were not related. Telomere length was associated with relapse, clonal evolution and mortality by using a multivariate analysis. The authors concluded by stating “In a cohort of patients with severe aplastic anemia receiving immunosuppressive therapy, telomere length was unrelated to response but was associated with risk of relapse, clonal evolution, and overall survival.”1

1Scheinberg P, Cooper JN, Sloand EM, et al. Association of telomere length of peripheral blood leukocytes with hematopoietic relapse, malignant transformation, and survival in severe aplastic anemia. JAMA. 2010;304(12):1358-64


Source: JAMA



Association Between Iron Deficiency Anemia and Ischemic Stroke.

Ischemia and infarction constitute 85-90 percent of strokes in western countries, with 10-15 percent being caused by intracranial hemorrhages. The morbidity and mortality from cerebrovascular diseases has actually decreased in recent years, due mostly to better recognition and treatment of underlying factors such as hypertension and cardiac diseases that increase the risk of stroke. More recently migraines have been found to increase the risk of ischemic stroke.

Anemia is often described as a decrease in the number of red blood cells (RBC) per mm3, or as a decrease in the hemoglobin concentration in blood to a level below the normal physiologic requirement that is necessary for adequate tissue oxygenation. Common causes include inadequate dietary intake, inadequate absorption from the GI tract (as in certain malabsorption syndromes, unrelenting diarrhea, or the presence of certain food or drugs), increased iron demands (as in pregnancy, adolescence, infancy, old age, or during exercise), blood loss, and certain diseases. Dietary deficiencies most frequently result from decreased consumption of animal protein and ascorbic acid, as a consequence of chronic alcoholism, food faddism, prolonged illness with anorexia, or poor nutrition.

A recent study examined the link between anemia and ischemic stroke in children. Previous research has found that iron deficiency anemia has a prevalence of 4-8% in children between the ages of one and three years and is associated with developmental delays, lethargy, irritability and cognitive issues. Occasionally, it appears that otherwise healthy children with severe iron deficiency anemia may be at an increased risk of ischemic stroke. The researchers found four cases of otherwise healthy children between the ages of 14 and 48 months with significant iron deficiency anemia in which three of the children had venous sinus thrombosis and one had arterial ischemic stroke. These results appear to confirm previous reports for a strong association between iron deficiency anemia and childhood stroke.1

1 Munot P, De Vile C, Hemingway C, et al. Severe iron deficiency anaemia and ischaemic stroke in children. Arch Dis Child. 2010.


Source: Archives of Disease in Childhood


Response of Peripheral and Central Nerve Pathology to Mega-Doses of the Vitamin B-Complex and Other Metabolites – Part 2

Recommended Treatment Schedule

Our treatment schedule:

1) Thiamin hydrochloride: 300mg to 500mg, 30 minutes before meals and bed hour, and during the night if awake. The higher amounts in long-standing cases. This requirement is high, since much is lost through action of gastric juices and loss due to perspiration. 400 mg. daily by needle, given intramuscularly. During summer months this can be given every 12 hours to good advantage. Two to three times each week, and where office access is convenient, 20 mg. per kg. body weight, or at least 1000 mg. is administered intravenously. This is given with 100 mg to 200 mg. Niacine (nicotinic acid) which is available 100 mg. in 10cc ampules. (The concentrated Niacin, available in 30cc vials, must be diluted if employed intravenously.) The intravenous dose is given with the patient in a recumbent position. A 20cc to 30cc syringe, carrying a one-inch 22-guage needle should be employed. The injection is given slowly (5 to 7 minutes) holding the syringe with one hand. The usually-employed three fingers of the other hand must be on the patient’s pulse. An increased pulse rate indicates too fast a flow of the medicine. This indicates the rate of phosphorylization. Thiamin hydrochloride is, indeed, a toxic substance, and anaphylactic reactions have been reported, but I have never seen a case in treating thousands of patients, (not necessarily Myasthenia Gravis or Multiple Sclerosis), in 30 years of clinical observation. I have observed one case of extreme sensitivity in which itching was present within One minute after an intramuscular injection of 100mg. This was immediately controlled with 5cc Benedryl, I.M. It must be remembered that once thiamin hydrochloride is phosphorylated, it is no longer a critical allergic substance, but is cocarboxylase, a necessary but absolutely harmless agent. (My problem has been the preservatives now required by FDA regulations, and they should be removed.) Higher doses of thiamin can be used, but then the dilution factor must be greater. (more…)

Chelating Iron in Conditions of Iron Overload (Hemochromatosis)

Iron is one of the most abundant earth elements, yet only traces are essential for living cells of plants and animals. In humans, most of the iron is contained within the porphyrin ring of heme in proteins such as hemoglobin, myoglobin, catalase, peroxidases, and cytochromes. as well as iron-sulfur proteins such as NADH dehydrogenase and succinate dehydrogenase, in which iron is present in clusters with inorganic sulfur. In all these systems, iron has the ability to interact reversibly with oxygen and to function in election transfer reactions that makes it biologically indispensable.

The average adult male contains approximately 4 grams of body iron. About 65% to 70% is found in hemoglobin, 4% in myoglobin, and less than 1% in other iron-containing enzymes and proteins. The remaining 25% to 30% represent the storage pool of iron. By contrast, women have a much smaller iron reserve, with the adult female body containing about 3 grams of iron. Women also have a slightly lower hemoglobin concentration in blood than males. Patients with iron overload diseases may store as much as 20 g of iron.

Excess iron can result in cell injury. Menstruation, bleeding due to injury, or bloodletting help to excrete excess iron. Other than that, humans do not excrete excess iron effectively.

Iron overload can result from an increased absorption of dietary iron or from parenteral administration of iron. When the iron burden exceeds the body’s capacity for safe storage, the result is widespread damage to the liver, heart, joints, pancreas, and other endocrine organs.1 It must be noted that low serum iron alone is not an indicator of iron deficiency. Serum ferritin, transferrin levels and total iron binding capacity must confirm the diagnosis before iron is supplemented. To improve iron absorption and utilization, adequate amounts of vitamins C and B, especially folic acid, B6, and B12, must be provided. (more…)

Iron Deficiency Anemia and Pregnancy.

Iron deficiency anemia occurs in approximately 25 percent of patients with anemia. Common causes include inadequate dietary intake, inadequate absorption from the GI tract (as in certain malabsorption syndromes, unrelenting diarrhea, or the presence of certain food or drugs), increased iron demands (as in pregnancy, adolescence, infancy, old age, or during exercise), blood loss, and certain diseases. Dietary deficiencies most frequently result from decreased consumption of animal protein and ascorbic acid, as a consequence of chronic alcoholism, food faddism, prolonged illness with anorexia, or poor nutrition. (more…)

The Importance of B Vitamins to Overall Health

B vitamins are essential to health. Your nerves, skin, eyes, hair, liver, mouth, muscles, gastrointestinal tract, and brain depend on them for proper functioning. They are coenzymes that are involved in energy production and are also useful for alleviation of depression and anxiety.

As we get older our ability to absorb B vitamins from our food declines. In some Alzheimer’s patients, it was found that the problem was due to a deficiency of vitamin B-12 plus vitamin B-complex in an accepted multivitamin. (more…)

Understanding the Serum Vitamin B12 Level and Its Implications for Treating Neuropsychiatric Conditions: An Orthomolecular Perspective

Vitamin B12 (cobalamin) ranks among the most useful, safe, and effective orthomolecules when treating a diverse array of neuropsychiatric conditions. However, most clinicians do not consider vitamin B12 important unless the serum level is below laboratory reference ranges. Ten research reports, summarized here, indicate metabolic consequences from low-normal (but not deficient) serum B12 levels, and/or clinical improvements following therapy that markedly increased serum B12 levels. My clinical experience, along with the summarized reports, suggests that (1) serum levels of vitamin B12 not “classically” deficient by current laboratory standards are associated with neuropsychiatric signs and symptoms, and (2) clinical improvement results when serum vitamin B12 levels are optimized or markedly increased following vitamin B12 treatment. Vitamin B12’s mechanisms of action are believed to include increased S-adenosylmethionine production, improved methylation, decreased plasma and brain homocysteine, compensation for inborn errors of metabolism, normalized gene expression, correction of long-latency vitamin B12 debt, and anti-inflammatory activity. Clinicians may wish to reevaluate the importance of lower-than-optimal serum vitamin B12 levels, pursue additional testing such as urinary methylmalonic acid, and consider the potential benefits of vitamin B12 treatment. (more…)