The term anemia does not describe a specific disease but rather a physical state. It is defined as decrease in either hemoglobin or red blood cells, or decreases in both. Iron is the essential component of hemoglobin, which in turn is the essential component of red blood cells. Red blood cells combine with oxygen in the lungs and carry the oxygen throughout the body. Anemia prevents an adequate distribution of oxygen, which thereby inhibits normal health activities.
Since there are many causes of anemia, only the following high incidence causes will be discussed: iron deficiency, vitamin B-12 deficiency, folic acid deficiency, hemolysis and sickling.
Iron deficiency anemia is worldwide and is the most common form of anemia, being most prevalent in women. This condition occurs when there is not enough iron in the body, with the result that inadequate amounts of hemoglobin are formed. Normal body iron supplies become low if dietary iron intake is low, if dietary iron is not absorbed, or if iron is not resorbed from old red blood cells. Although this anemia does not usually lead to death, taking self-prescribed medications may mask an underlying treatable disease. This becomes serious if it is the underlying disorder that must be cured to prevent continued iron deficiency anemia. Therefore, self-treatment is advised against.
Vitamin B-12 deficiency anemia results from a shortage of vitamin B-12 in the blood. Vitamin B-12 is involved in the production of red blood cells in bone marrow; anemia will therefore result if blood concentration of the vitamin is below normal. Vitamin B-12 functions in the cell nucleus; low levels cause whatever red blood cells form to be outsized and misshapen. If vitamin B-12 deficiency occurs because of malabsorption, normal blood concentrations will never return. Vitamin B-12 injections may be necessary for the remainder of the individual's life. This state occurs equally in men and women, and rarely occurs before age 40.
In folic acid anemia blood levels of folacin are abnormally low. As with vitamin B-12, folacin functions at the nuclear level in the formation of red blood cells with bone marrow. Unlike vitamin B-12 anemia, folic acid anemia may be treated simply by diet and/or folacin tablets.
Hemolytic anemia occurs when reproduction of new red blood cells is surpassed by the rate at which red blood cells are destroyed. Treatment may involve prescribed drugs, as in the case of antibody-produced anemia, discontinued use of drugs which enhance red blood cell destruction, or removal of the spleen whose normal function is to remove old red blood cells from the bloodstream.
Sickle cell anemia is an inherited condition in which red blood cells contain an abnormal hemoglobin called hemoglobin S. Hemoglobin S. causes the cells to be deformed or "sickle-shaped." This deformation prevents the smooth flow of blood through the circulatory system, causes blood vessels to clog, and creates a state of local anoxia. Furthermore, premature hemolysis may occur. Sickle cell anemia is virtually unknown except in Negroids and individuals from parts of Greece, India, Italy and Arabia. Because the disease causes difficulty in transporting oxygen to the body, individuals with this disease should not travel to high altitudes, nor should they travel in unpressurized airplanes. There is no cure at this time for sickle cell anemia. However, the symptoms may be treated. The best treatment is maintenance of good health, especially by following a good diet. In severe cases, hospital injected painkillers may be necessary.
Iron deficiency anemia
Increased metabolic iron requirements, such as during pregnancy
Inadequate dietary iron to replace that which is lost, especially in young children
Malabsorption of iron in the digestive tract occurring when part of the stomach has been removed or in celiac disease
Iron reserves depletion due to excessive blood loss; this is the most common cause of anemia, especially in women
Temporary losses, usually replenished quickly:
Heavy menstrual periods
Cancer of the large intestine
Vitamin B-12 deficiency anemia
Inability to absorb vitamin B-12; known as pernicious anemia, occurs due to the lack of a substance in the digestive tract called the intrinsic factor, and is the most common form of vitamin B-12 deficiency
Low levels of gastric acid
Surgical disturbance of the digestive tract
Strict vegetarian diets which preclude meat, fish, poultry, eggs and dairy products
Folic acid deficiency anemia
Inadequate dietary folacin
Celiac disease inability to absorb sufficient amounts of folacin
Metabolic needs for abnormally large amounts of folacin, more than provided by a normal diet
Heredity, when a specific component of red blood cells is abnormal
Predisposed hemolysis on the intake of certain drugs
Autoimmune attack against red blood cells
Immune attack against recently transfused red blood cells
Damage to red blood cells due to artificial heart parts, abnormal blood vessel walls, and toxins
Sickle cell anemia
This is a genetic disease which primarily occurs in homozygous recessive individuals.
Heterozygous individuals are said to have sickle cell trait and will often show no symptoms except under extreme circumstances.
Signs & Symptoms
All forms of anemia, especially during physical exertion:
Weakness Fatigue Paleness Dyspnea Heart flutters Heart palpitations Fainting spells or actual fainting Increased awareness of heartbeat due to a pounding pulse
Memory loss Confusion Indigestion Depression Inability to walk or keep proper balance Continuous tingling of the hands and feet
Yellowing of skin, due to an increase in bilirubin in the blood
Pernicious anemia may be hereditary.
Folic acid deficiency anemia
Alcoholism, since alcoholics tend to eat an unbalanced diet
Blood in urine Gallstones Jaundice Splenomegaly
Impaired blood circulation Fever Attacks of pain in the abdomen and bones Blood clots in the lung, kidney, brain, and most other organs lead to states of anoxia called sickle cell crises
Structure & Function: Circulatory Support
Adult Child/Adolescent Copper 2 - 5 mg 1 - 3 mg Folic acid 400 - 1,000 mcg 400 - 800 mcg Iron 20 - 50 mg 10 - 20 mg Methionine 500 - 1,000 mg 100 - 300 mg Molybdenum 100 - 300 mcg 50 - 200 mcg Spirulina* Vitamin B-6 10 - 25 mg 5 - 10 mg Vitamin B-12 500 - 1,000 mcg 100 - 300 mcg
* Please refer to the respective topic for specific nutrient amounts.
Recent advances in our understanding of essential fatty acids have led to an indication for fatty acids (e.g. fish oils/EPA) in some anemic conditions.
Other advances, in producing phosphatidylserine from soy, have made it more available for use, one indication being anemia.
Another plant food with an unusual range of nutrients may also be efficacious: spirulina.
All amounts are in addition to those supplements having a Recommended Dietary Allowance (RDA). Due to individual needs, one must always be aware of a possible undetermined effect when taking nutritional supplements. If any disturbances from the use of a particular supplement should occur, stop its use immediately and seek the care of a qualified health care professional.
The diet prescribed for anemia, the Protein Enriched Diet, is one which emphasizes the intake of iron and factors which assist in its absorption, such as vitamin C. Care should be taken to exclude dietary factors which would interfere with iron's absorption, such as tea (black) and phytates.
Iron deficiency anemia may cause acute iron depletion, for which a physician may prescribe iron tablets, iron injections, or simply a change in diet. In severe cases, a blood transfusion may be necessary. Large doses of iron many be toxic.
Vitamin B-12 deficiency anemia is not amenable to nutritional management. Treatment consists of the administration of vitamin B-12 shots.
Folic acid deficiency anemia can be due to the use of oral contraceptives, antimalarials or anticonvulsants, poor diet during pregnancy, steatorrhea, or faulty absorption of the vitamin from the diet.
Treatment consists of providing a Protein Enriched Diet with supplemental iron and vitamins. Some recommended foods for this diet are:
Dark green leafy vegetables
Vitamin C supplementation is also advised. Increasing the levels of this vitamin accelerates recovery from the anemia because vitamin C converts folacin into its biologically active form.
Hemolytic anemia can be due to a vitamin E deficiency. Supplementation with vitamin E decreases the fragility of the red blood cell.
Sickle cell anemia: During sickling crisis there is a profound destruction of red blood cells. The iron liberated is then deposited in organs such as the liver. To minimize this accumulation, the individual should adhere to a diet low in iron.
The diet should also be low in fats, for ease in digestion, since the functions of the liver and gallbladder are impaired in the disease.
Folacin is prescribed to aid in the production of new red blood cells; this can be obtained through diet with a dosage of 400 to 600 micrograms per day. Because this level may be hard to achieve through diet alone, a 250 microgram supplement is usually prescribed.
Lower plasma levels of vitamin B-6 were found in anemic individuals as compared to controls; individuals with sickle cell anemia may be deficient in vitamin B-6. These levels can be raised by supplementation of 100 milligrams per day for several months. 20% of those treated with vitamin B-6 experienced fewer and less severe crises during the study period.
Individuals with sickle cell anemia are often deficient in zinc as well. The kidney is overwhelmed by the large amount of zinc which is released by hemolysis during a crisis. The zinc is then hyperexcreted, rather than being resorbed into the bloodstream. The resultant lack of zinc accounts for poor wound healing experienced by these persons; zinc supplementation may improve healing.
Toxic anemia: Anemia due to acute copper toxicity can be produced by doses greater than 250 milligrams per day.
1. Cinchona officinalis tinct. 15 - 30C
2.* Calcarea phos. tinct. - 3X to 30X
3.* Ferrum phosphoricum - 3X (increases hemoglobin)
4.* Natrum muriaticum - 30C to 1M
Doses cited are to be administered on a 3X daily schedule, unless otherwise indicated. Dose usually continued for 2 weeks. Liquid preparations usually use 8-10 drops per dose. Solid preps are usually 3 pellets per dose. Children use 1/2 dose.
X = 1 to 10 dilution - weak (triturition)
C = 1 to 100 dilution - weak (potency)
M = 1 to 1 million dilution (very strong)
X or C underlined means it is most useful potency
Asterisk (*) = Primary remedy. Means most necessary remedy. There may be more than one remedy - if so, use all of them.
Boericke, D.E., 1988. Homeopathic Materia Medica.
Coulter, C.R., 1986. Portraits of Homeopathic Medicines.
Kent, J.T., 1989. Repertory of the Homeopathic Materia Medica.
Koehler, G., 1989. Handbook of Homeopathy.
Shingale, J.N., 1992. Bedside Prescriber.
Smith, Trevor, 1989. Homeopathic Medicine.
Ullman, Dana, 1991. The One Minute (or so) Healer.
Calc. Phos. 4 tablets every 2 hours.
Red raspberry plant
Note: The misdirected use of an herb can produce severely adverse effects, especially in combination with prescription drugs. This Herbal information is for educational purposes and is not intended as a replacement for medical advice.
Most herbal preparations recommended for anemia boost iron.
Blue vervain may be substituted for children.
Yellow dock may even be useful in sickle cell anemia.
Aromatherapy - Essential Oils
Chamomile Essence, Lemon Essence, Lavender Essence, Melissa Essence, Peppermint Essence, Rosemary Essence.
Related Health Conditions
Alcoholism Gastritis Angina pectoris Heart disorders Blood clots Hemorrhoids Cancer Jaundice Celiac disease Indigestion Depression Insufficient blood circulation Fainting Pregnancy Fatigue Splenomegaly Fever Ulcers Gallstones
Anonymous: ACOG educational bulletin. Nutrition and women. Number 229, October 1996. Committee on Educational Bulletins of the American College of Obstetricians and Gynecologists. Int J Gynaecol Obstet, 1997 Jan, 56:1, 71-81.
Ballentine, R. 1978. Diet And Nutrition. The Himalayan International Institute Pub., Honesdale, Pennsylvania. 634 pp
Bland, Jeffrey. Medical Applications of Clinical Nutrition. New Canaan, Conn.: Keats, 1983.
Eagles, J.A. & M.N. Randall. 1980. Handbook of Normal and Therapeutic Nutrition. Raven Press, New York. 323 pp.
Eichner, E. R. : Sports Anemia, Iron Supplements, and Blood Doping. Medicine and Science in Sports and Exercise, 1992;S315-S318.
Flanagan, P.R., J. Haist & L.S. Vasberg. Intestinal Absorption of Zinc: Competitive Interaction With Copper With Sex-Linked Anemia. Canadian Journal Of Physiological Pharmacology, 62 (1984).
Gallagh G & Ehrenz RA: Nutritional anemias in infancy. Clin Perinatol, 1995 Sep, 22:3, 671-92.
Gyorffy, E. J.and Chan, H.: Copper Deficiency and Microcytic Anemia Resulting From Prolonged Ingestion of Over-The-Counter Zinc. The American Journal of Gastroenterology, August 1992;87(8):1054-1055.
Hirase, Nobuhisa, et al: Anemia and Neutropenia in A Case of Copper Deficiency: Role of Copper in Normal Hematopoiesis. ACTA Hematologica, 1992;87:195-197.
Howe, P. S. 1981. Basic Nutrition in Health and Disease, 7th ed. W.B. Saunders Co., Philadelphia.
Hui, Y. H. 1983. Human nutrition and diet therapy. WadsWorth, Inc; Belmont, California. 1039 pp.
Isselbacher, K.J. & R.D. Adams. 1980. Harrison's Principles of Internal Medicine, 9th ed. McGraw Hill Book Company Pub, NY. 2073 pp.
Iwama, A. et al: Megaloblastic Anemia Associated With Psoriasis: Case Report and Review of the Literature, Internal Medicine, January 1992;31(1):127-130.
Johnson-Spear MA & Yip R: Hemoglobin difference between black and white women with comparable iron status: justification for race-specific anemia criteria [see comments].Am J Clin Nutr, 1994 Jul, 60:1, 117-21.
Kirschmann, J.D. 1990. Nutrition Almanac: Nutrition Search. McGrew-Hill: New York.
Kunz, J. R. M. 1982. The American Medical Association Family Medical Guide. Random House Pub, New York. 832 pp.
Luke, B. 1984. Principles of Nutrition and Diet Therapy. Little, Brown, and Co., Boston. 816 pp.
Looker AC et al., Prevalence of iron deficiency in the United States. JAMA, 1997 Mar 26, 277:12, 973-6.
Murray, M.T., & J.E. Pizzorno. 1991. Encyclopedia of Natural Medicine. Rocklin, Ca; Prima Publishing.
Natta, C. & R.D. Reynolds. 1984. Apparent vitamin B6 deficiency in sickle cell anemia. American Journal Of Clinical Nutrition. Vol.40.
Oski, F.A. The Nonhematologic Manifestations of Iron Deficiency. American Journal Of Disabilities In Children, 133 (1979).
Pegelow CH et al., Natural history of blood pressure in sickle cell disease: risks for stroke and death associated with relative hypertension in sickle cell anemia. Am J Med, 1997 Feb, 102:2, 171-7.
Rindi, G. et al.: Thiamine Transport by Erythrocytes and Ghosts in Thiamine-Responsive Megaloblastic Anemia Journal of Inher. Metab. Dis., 1992;15:231-242.
Robbins, S. L. & R. S. Cotran. 1979. Pathologic Basis of Disease, 2nd ed. Saunders Pub Co., Philadelphia. 1598 pp.
Subak-Sharpe, G. J. 1984. The Physician's Manual For Patients, Times Books Pub, New York. 607 pp.
Van Der Wyden, M.B. & H. Fong. Red Cell Ferritin Content of Patients With Megaloblastic Anemia Due to Vitamin B-12 and Folate Deficiency. Scandinavian Journal Of Hemology, 33 (1984).
Williams, J. Iron Deficiency Treatment. Western Journal Of Medicine, 134 (1981).
Williams R et al., Nutrition assessment in children with sickle cell disease. J Assoc Acad Minor Phys, 1997, 8:3, 44-8.
Winick, M. Nutritional Disorders Of American Women. N Y: Wiley, 1977.
Worthington-White DA et al., Premature infants require additional folate and vitamin B-12 to reduce the severity of the anemia of prematurity. Am J Clin Nutr, 1994 Dec, 60:6, 930-5.
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