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According to, Anemia is “one of the more common blood disorders. It occurs when the level of healthy red blood cells (RBCs) in the body becomes too low. This can lead to health problems because RBCs contain hemoglobin, which carries oxygen to the body's tissues. Anemia can cause a variety of complications, including fatigue and stress on bodily organs.” <ref></ref>

The term anemia refers to a decrease in the numbers of red blood cells (RBCs) or hemoglobin (Hb) content caused by a limited number of mechanisms that can function independently or occur synergistically. The term anemia is often used incorrectly as a diagnosis, but like hypertension, is really a symptom of an underlying pathology. Thus different types of anemia are defined according to the pathophysiology.

Someone who has anemia is called anemic.

The rate by which RBCs develop in red bone marrow is dependent upon the status of hemoglobin, which ensures the proper oxygenation of the tissues. This process is maintained by a negative feedback mechanism that is stimulated by hypoxic conditions in the affected tissues, which in turn, promotes an increase in RBC synthesis until tissue oxygen levels are restored to normal. RBCs develop from pluripotent hematopoietic stem cells to progenitor cells, when then form into proerythroblasts, reticulocytes and then erythrocytes (RBCs) in a process requiring a variety of growth factors and cytokines including erythropoietin. Once formed, RBC precursor cells are released into circulation as reticulocytes where they remain in circulation for about one day until they lose their nucleus. This causes the center of the cell to indent and form the distinctive concave shape of a mature RBC. Since erythrocytes have no nucleus they rely upon anaerobic and aerobic glycolytic pathways for energy, and as the cell ages the levels of these enzymes gradually decrease. After 120 days worn and damaged RBCs are destroyed by phagocytic cells in the liver and spleen. Thus the body requires that at least 1/120 the number of RBCs are produced on a daily basis to maintain homeostasis and prevent hypoxia. (Berkow 1992; Rubin and Farber 1990, 553-563)

The unique concave shape of an RBC functions to increase the surface area for gas exchange. This shape also ensures that RBCs are highly deformable, and can bend in upon themselves allowing them to squeeze through the narrow openings of capillaries into the tissues. Each RBC contains approximately 280 million molecules of hemoglobin (Hb), contained in a lipid membrane and supported by a cytoskeletal network. (Berkow 1992; Rubin and Farber 1990, 553-563)

Generally speaking, there are three primary causes of anemia:

  • blood loss
  • deficient erythropoiesis (decreased production of RBCs)
  • excessive hemolysis (increased RBC destruction)

A number of conditions can cause anemia, including:

  • external blood loss: e.g. trauma, injuries, menorrhagia, and stomach ulcers
  • iron deficiency: iron is an important component in the production of [hemoglobin
  • chronic disease: any long-term disease can lead to anemia
  • kidney disease: through decreased erythropoietin secretion
       pregnancy: water gain during pregnancy is thought to dilute the RBCs (hemodilution); the fetus also robs the mother of iron during pregnancy
       poor nutrition: inadequate source of dietary iron and accessory nutrients (e.g. B complex); also common in alcoholism (Berkow 1992)

More uncommon causes of anemia include bleeding disorders, liver disease, thalassemia, infection, cancer, arthritis, enzyme deficiency, sickle cell disease, hypothyroidism, toxins, or hereditary conditions.

Signs and symptoms of anemia include:

   black and tarry stools (sticky and foul smelling)
   maroon, or visibly bloody stools
   rapid heart rate
   rapid breathing
   pale or cold skin
   heart murmur
   chest and/or abdominal pain
   weight loss
   vertigo and fainting, especially upon standing

Apart from external blood loss from trauma or injury, the two primary metabolic mechanisms of anemia are deficient RBC production and excessive RBC destruction. (Berkow 1992; Rubin and Farber 1990, 553-563) Deficient erythropoiesis

Anemia is often classified according to RBC morphology, which can give an indication of the cause of the anemia, and thus terms such as microcytic anemia, normochromic-normocytic anemia, and macrocytic anemia are often used. These terms describe the different kinds of anemias that are caused by deficient erythropoiesis.

Microcytic anemia indicates an alteration in heme or globin synthesis, such as in iron deficiency, thalassemia (and related Hb-synthesis defects), and anemia of chronic diseases (e.g. infection, inflammation). Iron-deficiency anemia is the most common anemia, and is a chronic condition characterized by small, pale RBCs and iron depletion. The most common cause is blood loss, from chronic bleeding (e.g. erosive gastritis), excessive menstruation, or from a developing fetus. Other prominent causes include a dietary deficiency of iron, malabsorption from intestinal damage (e.g. inflammatory bowel disease or bowel surgery), or from the excess consumption of iron-chelating agents in diet (e.g. phytates in cereals and legumes, tannins and oxalates in certain plants, etc.). The most common clinical presentation is fatigue, dizziness, headache, insomnia pallor, weight loss and poor immunity. The conjunctiva, buccal mucosa and nail bed may be pale. In severe cases the patient may display pica (a craving for dirt, paint, chalk, glue, hair or ice), glossitis (inflammation of the tongue), cheilosis (sores about the lips and mouth), and koilonychia (thinning, concave nails). (Berkow 1992)

Normochromic-normocytic anemia refers to state of the RBCs that appears otherwise normal upon microscopic examination, but are diminished in number. Thus, this type of anemia suggests a failure to produce the necessary number of RBCs to accommodate those that are no longer viable and are removed from circulation by the spleen and liver. Normochromic-normocytic anemia is either hypoproliferative or hypoplastic. Hypoproliferative anemia is caused by a deficient production of erythropoietin (EPO), commonly associated with renal disease (which produces EPO), hypometabolic states (e.g. hypothyroidism), and protein deficiency. In contrast, hypoplastic or aplastic anemia results from a loss of RBC precursors due to a defect in the stem cell pool or an injury to the red marrow from which the RBCs are generated. The cause of such anemias are typically related from exposure to certain industrial chemicals (e.g. benzene, inorganic arsenic), radiation, or drugs (e.g. chemotherapy, antibiotics, NSAIDs, anticonvulsants). In some cases the cause is unknown and termed idiopathic aplastic anemia. (Berkow 1992)

Macrocytic or megablastic anemia refers to a state of deficient RBC production, but one in which the RBCs appear unusually large. This results from defective DNA synthesis but with continued RNA synthesis, resulting in an increase in RBC cytoplasmic mass. This form of anemia is typically related to a dietary deficiency or impaired metabolism vitamin B12 and/or folic acid (folate), as well as the use of cytotoxic and immunosuppressant drugs that impair proper DNA synthesis. (Berkow 1992)

A vitamin C deficiency can also promote anemia, usually associated with hypochromic anemia, but also normocytic and occasionally microcytic anemia. Vitamin C plays a key role in iron utilization. (Berkow 1992) Excessive hemolysis

Excessive hemolysis refers to the excessive destruction of RBCs, usually by phagocytic cells in the spleen, liver, and bone marrow. There are a variety of factors that promote the destruction of RBCs including defects in the RBC itself, or external factors such as the presence of anti-RBC immunoglobulins, trauma or infectious disease. Depending upon the cause, excessive hemolysis can be acute, chronic, or periodic.

A common clinical or laboratory finding for hemolysis is jaundice, occurring when the conversion of Hb to bilirubin exceeds the liver's capacity to form bilirubin glucuronide and excrete it into the bile, promotiong unconjugated bilirubinemia. Increased catabolism is also manifested by an increase in stercobilin in the stool and urobilinogen in the urine, as well as pigment-gallstones particularly in the course of the condition is chronic.

Abnormalities within the RBC that promote hemolysis are either related to some dysfunction within the cell or the cell membrane. There are a number of rare, congenital red cell membrane disorders including hereditary spherocytosis, congenital hemolytic jaundice, chronic acholuric jaundice, familial spherocytosis and spherocytic anemia. Acquired red cell membrane disorders include as stomatocytosis (caused by alcoholism) and hypophosphatemia (caused by several factors including starvation, diabetic acidosis, diuretics, vomiting, corticosteroids etc.), the latter of which results in RBC ATP depletion. ((Berkow 1992; Rubin and Farber 1990, 553-563)

Anemias caused by disorders of red cell metabolism relate to a failure of the RBC to use glucose effectively to produce ATP and are rare genetic disorders. Anemias caused by defective hemoglobin synthesis are similarly caused by genetic abnormalities. Sickle cell anemia is a RBC defect that is found mostly in people of African descent, and to a lesser extent those of Mediterranean and Middle Eastern descent. It characterized by a sickle-shaped RBC caused by the homozygous inheritance of Hb S, an abnormal form of hemoglobin that clumps together, making RBCs sticky, stiff, and more fragile, causing them to assume a curved, sickle shape. The distorted and inflexible RBCs adhere to vascular endothelium and end up plugging small arterioles and capillaries, leading to occlusion, hypoxia and local cell death. There are a variety of other congenital diseases that relate to impaired or improper hemoglobin synthesis and cause anemia, including hemoglobin C disease, hemoglobin S-C disease, and hemoglobin E disease. Of note is the relatively common thalassemia major and thalassemia minor, a group of chronic, inherited, microcytic anemias characterized by defective Hb synthesis and ineffective erythropoiesis resulting from decreased production of beta, alpha, gamma, or delta polypeptide chains. Thalassemia is particularly common in persons of Mediterranean, African, and Southeast Asian ancestry. (Berkow 1992; Rubin and Farber 1990, 553-563)

Hemolysis caused by defects external to the red cell is determined when no intrinsic RBC abnormality can be identified. Causes include:

   Hypersplenism: characterized by a mechanism that produces splenomegaly (splenic enlargement) with increased filtering of RBCs and phagocytic function. Mechanisms include infection (e.g. bacterial endocarditis, mononucleosis), hereditary conditions (e.g. spherocytosis, thalassemia major), congestive conditions (e.g. splenic vein thrombosis, portal hypertension), myeloproliferative disease (e.g. chronic myeloid metaplasia), infiltrative diseases (e.g. sarcoidosis) and cancer (e.g. chronic lymphocytic leukemia, lymphomas).
   Autoimmune hemolytic anemia (AIHA): identified by the presence of anti-RBC immunoglobulins. More frequent in women than in men, usually with an abrupt onset, producing a severe and potentially fatal anemia.
   Traumatic hemolytic anemia: caused by some kind of trauma such as hand-drumming or karate, or from roughened endothelial surfaces in the heart (e.g. calcific aortic stenosis) or arterioles (atherosclerosis); in the latter case, increases in blood pressure can also promote RBC damage
   Infectious hemolytic anemia: from reacting to toxins produced by infectious organisms in the body (e.g. Clostridium perfringens, hemolytic streptococci, meningococci), or when RBCs are actually infected themselves (e.g. Plasmodium and Bartonella spp.). (Berkow 1992; Rubin and Farber 1990, 553-563)

Holistic treatment

The cause of anemia must be carefully ascertained. From a herbal perspective, botanicals that nourish blood are indicated in every kind of anemia, regardless of cause, including Ashwaganda (Withania somnifera), Asparagus (Asparagus officinalis), Amalaki (Phyllanthus emblica), Dong Quai (Angelica sinensis), Gou Qi Zi (Lycium barbarum), Bai Shao (Paeonia lactiflora), and He Shou Wu (Polygonum multiflorum). Such herbs can be prepared as a strong decoction (1:1), strained well, and preserved with a combination of honey and molasses, taken in tablespoon-full doses bid-tid. Additional helpful herbs include Yellowdock (Rumex crispus), Raspberry (Rubus idaeus), and Nettle (Urtica dioica), as infusion or tincture.

   Microcytic anemia relates to an iron deficiency, caused by dietary a dietary deficiency of iron, malabsorption from intestinal damage (e.g. inflammatory bowel disease or bowel surgery), or from the excess consumption of iron-chelating agents in diet. Holistic treatment consists of increasing iron containing foods (e.g. meat, yams, figs, collard greens), botanicals that nourish blood, ascorbic acid and the B vitamins.
   Normochromic-normocytic anemia relates to either hypoproliferative causes (e.g. renal disease, hypothyroidism or protein deficiency), or hypoplastic causes (e.g. industrial chemicals, radiation, chemotherapy, antibiotics, NSAIDs, anticonvulsants. In each case the cause must be treated separately, but can also be treated generally with iron containing foods (e.g. meat, yams, figs, collard greens), botanicals that nourish blood, ascorbic acid and the B vitamins.
   Macrocytic or megablastic anemiarefers to a state of deficient RBC production, related to a deficiency or defective utilization of cobalamin or folic acid, and the use of cytotoxic and immunosuppressant drugs that interfere with DNA synthesis. Supplement with cobalamin (1000 mcg daily), folic acid (1 mg daily), along with the other B vitamins (100 mg daily), vitamin C (2-3 g daily), iron containing foods (e.g. meat, yams, figs, collard greens), and botanicals that nourish blood.

For the hemolytic anemias treatment is once again orientated to the cause, in addition to blood nourishing botanicals. Hemolytic anemias caused by autoimmunity require the use of anti-inflammatory and immunomodulating botanicals. For sickle-cell anemia specifically, Prickly Ash (Zanthoxylym clavaherculis) bark can be taken continuously, 20-40 gtt of a 1:5 tincture, bid-tid.

In this case “yam” refers to the true yam (Dioscorea spp.), not sweet potato which many people call a yam (Ipomoea batatas).

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Modern medicine has delineated several types of anemia: iron-deficiency anemia, pernicious anemia, sickle-cell anemia, and hypoproteinemic anemia (lack of protein in the blood), as well as certain vitamin-deficiency anemias, such as B-12 and folic acid deficiency anemia. Certain bleeding disorders, such as profuse menstrual bleed­ing (menorrhagia), bleeding hemorrhoids (or piles, arsha in Sanskrit), or bleeding gums, can lead to anemia because of blood loss. Whenever modern medicine deals with the problem of anemia, it considers all these etiological factors.

Ayurveda looks at anemia quite differ­ently. Ayurvedic classification of anemia falls under three basic doshic conditions: vata type, pitta type, and kapha type. It doesn't matter whether a person has iron deficiency or folic acid deficiency, what is important is how the anemia is expressing itself through a particular individual. As it turns out (see box page 123), there is also a correspondence between the Ayurvedic interpretation and the understanding according to modern medicine.

p. 122 Secrets of Ayurvedic Self-healing TYPES OF ANEMIA In vata-type anemia, the person looks thin, with dry skin, rough, scaly skin, and has cracking of the joints. He or she looks emaciated and has pale complexion, may suffer from breathlessness and constipation, and may pass tarry black stool.

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Vaidya Vasant Lad, BAMS, MAsc, Ayurvedic Institute Herb Seminars, Ayurvedic Institute, 1994-2002:

Vaidya Vasant Lad, BAMS, MAsc, Ayurvedic Institute Gurukula Notes, Ayurvedic Institute, 1994-2006

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Anemia Vata Diseases Vata Symptoms Diseases

anemia.txt · Last modified: 2018/02/26 18:10 (external edit)